Journal of Respiratory Biology and Translational Medicine - Journal

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class="book-item"> <div class="my-body-container"> <div class="d-flex align-items-start pb-1 pt-3"> <div class="articles-img align-self-start"> <div class="journals-cover article-img mb-2"> <a href="/uploads/2024/05/28/171687517164sw.jpg" data-lightbox="image-4" data-title=""> <img src="/uploads/2024/05/28/171687517164sw.jpg" alt="Journal of Respiratory Biology and Translational Medicine -logo"> </a> </div> </div> <div class="flex-grow-1 pl-5 pb-2"> <div class="d-flex justify-content-center"> <div class="left-title"> <h1 class="d-flex justify-content-between align-items-center"> Journal of Respiratory Biology and Translational Medicine <a class="orange-color mb-0" href="/journals/jrbtm/apc"> <img src="/style/image/open_access.png"> Open Access </a> </h1> <div class="d-flex"> <div class="flex-grow-1"> <div class="right-title d-flex align-items-center"> <p class="text-right mr-2">ISSN: 3006-6514 <span>(Online)</span></p> <p class="text-right mr-2">3006-6506 <span>(Print)</span></p> <p class="text-right mr-2"></p> </div> <div class="item-text"> <strong>An Official Journal of <a href="https://mycala.org/#home">Chinese-American Lung Association</a></strong><br /> <br /> <em>Journal of Respiratory Biology and Translational Medicine</em> is an open access, peer-reviewed online journal that publishes basic, clinical, and translational lung and respiratory research. It is published quarterly online by SCIEPublish. </div> </div> </div> </div> </div> </div> </div> </div> </section> <section class="mb-3 book-column"> <div class="my-body-container padding0"> <div class="book-item-fixed default-hide pt-2 pb-2"> <div class="d-flex align-items-center"> <div class="left-logo mr-3"> <a href="/" alt="Back to the homepage"> <svg xmlns="http://www.w3.org/2000/svg" class="navbar-logo" xml:space="preserve" version="1.0" viewBox="0 0 5.08 1.933"> <path d="M1.021 1.245a.29.29 0 0 1-.211-.054l-.027-.023-.003-.003.056-.066.003.004a.3.3 0 0 0 .043.033.2.2 0 0 0 .128.027l.024-.007.019-.01a.07.07 0 0 0 .022-.032.1.1 0 0 0 0-.036l-.004-.014a.1.1 0 0 0-.016-.02.1.1 0 0 0-.027-.017L.994 1.01.919.98a.3.3 0 0 1-.076-.05.14.14 0 0 1-.034-.067.2.2 0 0 1 0-.06.13.13 0 0 1 .027-.056.2.2 0 0 1 .049-.041A.2.2 0 0 1 .95.683a.3.3 0 0 1 .07-.001.2.2 0 0 1 .06.017.3.3 0 0 1 .075.05l.003.003-.05.061L1.103.81a.2.2 0 0 0-.053-.034.2.2 0 0 0-.063-.013.1.1 0 0 0-.046.008L.925.78a.06.06 0 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<div class="section-heading border-top-0"> <h3 class="section-title"> Editor-in-Chief </h3> </div> <ul class="row mt-3"> <li class="col pb-2 mb-2"> <div class="d-flex align-items-center height100"> <div class="avatar-container"> <a class="avatar-img" href="/journals/jrbtm/editors"> <img src="/uploads/2023/10/19/16976868055xhg.jpg" class="avatar img-thumbnail"> </a> </div> <div class="flex-grow-1 ml-3"> <h5>Prof. Dr. Jianwen Que</h5> <p>Department of Medicine, Columbia Center for Human Development, Columbia University Medical Center, New York, NY, USA</p> </div> </div> </li> </ul> </div> </section> <section class="articles-list1 mb-3"> <div class="my-body-container padding0"> <div class="section-heading"> <h3 class="section-title"> Articles <span>(23)</span> <a class="right" href="/journals/jrbtm/articles" target="_blank"> All articles <svg xmlns="http://www.w3.org/2000/svg" width="12" height="12" fill="currentColor" class="bi bi-chevron-double-right" viewBox="0 0 16 16"> <path fill-rule="evenodd" d="M3.646 1.646a.5.5 0 0 1 .708 0l6 6a.5.5 0 0 1 0 .708l-6 6a.5.5 0 0 1-.708-.708L9.293 8 3.646 2.354a.5.5 0 0 1 0-.708z"/> <path fill-rule="evenodd" d="M7.646 1.646a.5.5 0 0 1 .708 0l6 6a.5.5 0 0 1 0 .708l-6 6a.5.5 0 0 1-.708-.708L13.293 8 7.646 2.354a.5.5 0 0 1 0-.708z"/> </svg> </a> </h3> </div> <ul class="nav nav-tabs mt-2"> <li class="nav-item"><a class="nav-link active" id="all-tab" data-toggle="tab" href="#id-all">Latest published</a></li> <li class="nav-item"><a class="nav-link" id="downloaded-tab" data-toggle="tab" href="#id-downloaded">Most downloaded</a></li> <li class="nav-item"><a class="nav-link" id="popular-tab" data-toggle="tab" href="#id-popular" role="tab">Most popular</a></li> </ul> <div class="tab-content" id="myTabContent"> <div class="tab-pane fade show active" id="id-all"> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Commentary</h4> <span>16 December 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/368">State of the ART: Drug Screening Reveals Artesunate as a Promising Anti-Fibrosis Therapy</a> </h3> <p class="article-abseract clamp">Fibrosis is a progressive pathological process that severely impairs normal organ function. Current treatments for fibrosis are extremely limited, with no curative approaches available. In a recent article published in <i>Cell</i>, Zhang and colleagues employed drug screening using ACTA2 reporter iPSC-derived cardiac fibroblasts and identified artesunate as a potent antifibrotic drug by targeting MD2/TLR4 signaling. This study provides new insights into strategies for exploiting existing drugs to treat fibrosis.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YujieQiao" target="_blank"> Yujie Qiao </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JiurongLiang" target="_blank"> Jiurong Liang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=DianhuaJiang" target="_blank"> Dianhua Jiang* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/12/16/71652036b48f4b9a17ba1c1ceaec7967.jpg" data-lightbox="image-1" data-title=""><img src="/uploads/2024/12/16/71652036b48f4b9a17ba1c1ceaec7967.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Review</h4> <span>09 December 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/360">The Multifaceted Roles of Neutrophil Death in COPD and Lung Cancer</a> </h3> <p class="article-abseract clamp">Chronic obstructive pulmonary disease (COPD) and lung cancer are closely linked, with individuals suffering from COPD at a significantly higher risk of developing lung cancer. The mechanisms driving this increased risk are multifaceted, involving genomic instability, immune dysregulation, and alterations in the lung environment. Neutrophils, the most abundant myeloid cells in human blood, have emerged as critical regulators of inflammation in both COPD and lung cancer. Despite their short lifespan, neutrophils contribute to disease progression through various forms of programmed cell death, including apoptosis, necroptosis, ferroptosis, pyroptosis, and NETosis, a form of neutrophil death with neutrophil extracellular traps (NETs) formation. These distinct death pathways affect inflammatory responses, tissue remodeling, and disease progression in COPD and lung cancer. This review provides an in-depth exploration of the mechanisms regulating neutrophil death, the interplay between various cell death pathways, and their influence on disease progression. Additionally, we highlight emerging therapeutic approaches aimed at targeting neutrophil death pathways, presenting promising new interventions to enhance treatment outcomes in COPD and lung cancer.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=ArabellaWan" target="_blank"> Arabella Wan </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=DongshiChen" target="_blank"> Dongshi Chen* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/12/09/c75770e3d04dbae89fd97c14bc426033.jpg" data-lightbox="image-2" data-title=""><img src="/uploads/2024/12/09/c75770e3d04dbae89fd97c14bc426033.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Meeting Report</h4> <span>04 December 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/356">Progress and Gaps in Respiratory Disease Research and Treatment: Highlights of the IRM 2024 in Shanghai</a> </h3> <p class="article-abseract clamp">Respiratory diseases pose a major public health challenge globally, necessitating collaborative efforts between basic researchers and clinicians for effective solutions. China, which is heavily impacted by a broad spectrum of respiratory disorders, has made notable strides in both research and clinical management of these diseases. The International Respiratory Medicine (IRM) meeting was organized with the primary goal of facilitating the exchange of recent research developments and promoting collaboration between Chinese and American scientists in both basic and clinical research fields. This article summarizes key insights from IRM2024, held in Shanghai, where a wide range of topics were discussed, including lung tissue development, disease mechanisms, and innovative therapeutic strategies. By integrating perspectives from basic, translational, and clinical research, IRM2024 highlighted recent advancements, addressed persistent challenges, and explored future directions in respiratory science and clinical practice. The insights gained from IRM2024 are poised to be pivotal in shaping future research and therapeutic approaches, further reinforcing the global commitment to enhancing respiratory health and improving patient outcomes.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Jin-SanZhang" target="_blank"> Jin-San Zhang* </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=QhaweniDhlamini" target="_blank"> Qhaweni Dhlamini </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=QiangGuo" target="_blank"> Qiang Guo </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=MeiyuQuan" target="_blank"> Meiyu Quan </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JinWu" target="_blank"> Jin Wu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HandengLyu" target="_blank"> Handeng Lyu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=LeiChong" target="_blank"> Lei Chong </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YuqingLv" target="_blank"> Yuqing Lv </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YutingLin" target="_blank"> Yuting Lin </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=BinZhou" target="_blank"> Bin Zhou </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YuruLiu" target="_blank"> Yuru Liu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HonglongJi" target="_blank"> Honglong Ji </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=XinhuaLin" target="_blank"> Xinhua Lin </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=WenNing" target="_blank"> Wen Ning </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=PengfeiSui" target="_blank"> Pengfei Sui </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HuaiyongChen" target="_blank"> Huaiyong Chen </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=PeisongGao" target="_blank"> Peisong Gao </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=WeiChen" target="_blank"> Wei Chen </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=XiaoboZhou" target="_blank"> Xiaobo Zhou </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YuanlinSong" target="_blank"> Yuanlin Song </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=ChaoqunWang" target="_blank"> Chaoqun Wang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=XiaoSu" target="_blank"> Xiao Su </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JinfuXu" target="_blank"> Jinfu Xu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JieSun" target="_blank"> Jie Sun </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YinChen" target="_blank"> Yin Chen </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YanGeng" target="_blank"> Yan Geng </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HaiSong" target="_blank"> Hai Song </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HongbinJi" target="_blank"> Hongbin Ji </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YuanpuPeter Di" target="_blank"> Yuanpu Peter Di </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HaoTang" target="_blank"> Hao Tang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=ChaoLu" target="_blank"> Chao Lu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JinghongLi" target="_blank"> Jinghong Li </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=KeCheng" target="_blank"> Ke Cheng </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=MengshuCao" target="_blank"> Mengshu Cao </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JiurongLiang" target="_blank"> Jiurong Liang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YingzeZhang" target="_blank"> Yingze Zhang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YangZhou" target="_blank"> Yang Zhou </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YingXi" target="_blank"> Ying Xi </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=WeiningXiong" target="_blank"> Weining Xiong* </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=BinCao" target="_blank"> Bin Cao* </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JianwenQue" target="_blank"> Jianwen Que* </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=DianhuaJiang" target="_blank"> Dianhua Jiang* </a> </div> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Review</h4> <span>02 December 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/354">The Interplay of Heart Failure and Lung Disease: Clinical Correlations, Mechanisms, and Therapeutic Implications</a> </h3> <p class="article-abseract clamp">Heart failure (HF) is a common clinical syndrome marked by reduced cardiac output, elevated intracardiac pressures, and heart dysfunction. Chronic HF (CHF) is a syndrome characterized by a lack of blood flow and impaired pumping ability to the heart over time, while acute HF (AHF) arises suddenly due to incidents like myocardial infarction or cardiac arrest. HF has a significant impact on pulmonary health and function, leading to conditions such as pulmonary edema and restrictive lung patterns. Clinical evidence highlights the bidirectional relationship between HF and lung dysfunction. Declining lung function serves as a predictor for HF progression and severity, while HF contributes to worsening lung health. Animal models that induce HF through surgical methods further demonstrate the connection between heart and lung pathology. The main mechanisms linking HF and lung dysfunction are pressure overload and chronic systemic inflammation, with changes in the extracellular matrix (ECM) also playing a role. Additionally, environmental factors like air pollution exacerbate lung inflammation, increasing the risk of both HF and chronic obstructive pulmonary disease (COPD) incidence. Combined treatment approaches involving pharmaceutical drugs such as statins, Angiotensin-converting enzyme (ACE) inhibitors, and Angiotensin receptor blockers (ARBs) may benefit by reducing inflammation. This review will explore the complex interplay between HF and lung function, emphasizing their interconnected pathophysiology and potential integrated treatment strategies.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=SalmaAhmad" target="_blank"> Salma Ahmad </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=AymanIsbatan" target="_blank"> Ayman Isbatan </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=SunnyChen" target="_blank"> Sunny Chen </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=StevenM.Dudek" target="_blank"> Steven M. Dudek </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=RichardD.Minshall" target="_blank"> Richard D. Minshall </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JiwangChen" target="_blank"> Jiwang Chen* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/12/02/0067734306b022460afa54c3951433e6.jpg" data-lightbox="image-4" data-title=""><img src="/uploads/2024/12/02/0067734306b022460afa54c3951433e6.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Review</h4> <span>15 November 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/337">Ion Channels in the Immune Response of Asthma</a> </h3> <p class="article-abseract clamp">Asthma is a common respiratory disorder characterized by chronic inflammation of the lower airways, contributing to significant morbidity, mortality, and a substantial global economic burden. It is now understood as a heterogeneous condition, with ongoing research shedding light on its complex immunological underpinnings. Ion channels, which are specialized transmembrane proteins that facilitate ion movement based on electrochemical gradients, play a crucial role in the pathophysiology of asthma. Ion channels regulate essential processes like maintaining epithelial hydroelectrolyte balance and also play a role in modulating immune responses involved in asthma. We discuss the connection between ion channel activity and immune regulation in asthma, focusing on ion channel regulation of immune cell behavior, airway hyperresponsiveness, and inflammation in asthma. Understanding ion channels in asthma could lead to the development of targeted therapies modulating their activity, thereby enhancing disease management and patient outcomes.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=LiangYan" target="_blank"> Liang Yan </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=LuZhang" target="_blank"> Lu Zhang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=KennethOgunniyi" target="_blank"> Kenneth Ogunniyi </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=LiangHong" target="_blank"> Liang Hong* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/11/18/0e3d431294bb40a86ebce8e27d7a2c10.png" data-lightbox="image-5" data-title=""><img src="/uploads/2024/11/18/0e3d431294bb40a86ebce8e27d7a2c10.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>04 November 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/328">Diversity and Meta-Analysis of Microbial Differential Abundance in Nasal Metatranscriptomic Profiles of Asthma</a> </h3> <p class="article-abseract clamp">Asthma affects millions worldwide and involves complex genetic, immunological, and environmental factors. The nasal microbiome is increasingly recognized for its role in asthma development, but inconsistent results and small sample sizes have limited a clear understanding. We aimed to clarify the nasal microbiome’s role in asthma using large datasets and meta-transcriptomic analysis. RNA-seq data was analyzed from two large public studies: GALA II (694 children of Puerto Rican heritage; 441 asthmatics, 253 controls) and CAAPA (562 individuals of African ancestry; 265 asthmatics, 297 controls). After quality control and host read removal, microbial reads were annotated using Kraken2. α and β diversity analyses compared microbial diversity between asthmatic and control groups. Differential abundance analysis was conducted separately, controlling for age and sex, with results combined via meta-analysis. We found that asthmatic patients exhibited significantly higher α diversity indices (Shannon, Berger-Parker, Inverse Simpson, Fisher’s) in nasal microbiota compared to controls in GALA II, with similar trends in CAAPA. β diversity analysis showed significant differences in microbial composition in GALA II data. Differential abundance analysis identified 20 species in GALA II and 9 species in CAAPA significantly associated with asthma. Meta-analysis revealed 11 species significantly associated with asthma, including <i>Mycobacterium_tuberculosis.</i> Our study demonstrates increased nasal microbiome α diversity in asthmatic patients and identifies specific microbial species associated with asthma risk. These findings enhance understanding of asthma pathogenesis from the nasal microbiome perspective and may inform future research and therapeutic strategies.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=AndrewLi" target="_blank"> Andrew Li </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=MolinYue" target="_blank"> Molin Yue </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=XiangyuYe" target="_blank"> Xiangyu Ye </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=KristinaGaietto" target="_blank"> Kristina Gaietto </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=AnnaF.Wang-Erickson" target="_blank"> Anna F. Wang-Erickson </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=WeiChen" target="_blank"> Wei Chen* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/11/04/8d97ec9dd39763e9f855648c317f0718.png" data-lightbox="image-6" data-title=""><img src="/uploads/2024/11/04/8d97ec9dd39763e9f855648c317f0718.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>11 October 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/300">Surfactant Protein-C Regulates Alveolar Type 2 Epithelial Cell Lineages via the CD74 Receptor</a> </h3> <p class="article-abseract clamp">Deficiency of surfactant protein-C (SPC) increases susceptibility to lung infections and injury, and suppressed expression of SPC has been associated with the severity of acute respiratory distress syndrome (ARDS). Alveolar type 2 epithelial cells (AT2) are critical for maintenance and repair of the lung. However, the role of the SPC in the regulation of AT2 cell lineage and the underlying mechanisms are not completely understood. This study aimed to investigate the mechanisms by which SPC regulates AT2 lineages. <i>Sftpc−/− </i>mice were used to model the SPC deficiency in ARDS patients. We utilized three-dimensional (3D) organoids to compare AT2 lineage characteristics between wild type (WT) and <i>Sftpc−/− </i>mice by analyzing AT2 proliferation, alveolar type 1 cells (AT1) differentiation and CD74 expression, using colony-formation assay, immunofluorescence, flow cytometry, and immunoblots. The results showed that <i>Sftpc</i>−/− mice demonstrated a reduced AT2 cell population. Influenza A virus subtype H1N1 (H1N1) infected <i>Sftpc−/− </i>mice demonstrated reduced AT2 proliferation and AT1 differentiation. Western blot indicated elevated levels of CD74 protein in AT2 cells of <i>Sftpc−/− </i>mice. Colony-forming efficiency was significantly attenuated in AT2 cells isolated from <i>Sftpc−/− </i>mice compared to the WT controls. Podoplanin (PDPN, a marker of AT1 cells) expression and transient cell count significantly increased in <i>Sftpc−/− </i>organoids. Moreover, siRNA-mediated gene silencing of CD74 in AT2 cells significantly increased AT2 proliferation and AT1 differentiation in <i>Sftpc−/− </i>organoids. This study suggests that SPC regulates AT2 lineage in vitro and in vivo. The SPC might influence AT2 lineage during the lung epithelium repair by activating signaling mechanism involving CD74 receptor.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=KrishanG.Jain" target="_blank"> Krishan G. Jain* </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YangLiu" target="_blank"> Yang Liu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=RunzhenZhao" target="_blank"> Runzhen Zhao </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=PreetiJ.Muire" target="_blank"> Preeti J. Muire </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Nan-MilesXi" target="_blank"> Nan-Miles Xi </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Hong-LongJi" target="_blank"> Hong-Long Ji* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/10/11/5e8caa6a23316115d46d6ec32df71303.jpg" data-lightbox="image-7" data-title=""><img src="/uploads/2024/10/11/5e8caa6a23316115d46d6ec32df71303.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>27 September 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/290">Evaluation of the Efficacy of Chinese Inactivated COVID-19 Vaccines against the Delta Variant in the Nanjing Outbreak: A Cohort Study</a> </h3> <p class="article-abseract clamp">Background: The strains of COVID-19 are constantly mutating, and the effectiveness of Chinese inactivated vaccines against the COVID-19 Delta variant has not been described clearly. Methods: The clinical data of patients with the COVID-19 Delta variant in the 2021 Nanjing outbreak were retrospectively reviewed. Results: There were 212 patients with the COVID-19 Delta variant (unvaccinated, <i>n </i>=<i> </i>56, 26.42%; vaccinated, <i>n </i>=<i> </i>156, 73.58%) included in our cohort study. The median age was 45.5 (38, 53) years old. Eighty-seven subjects (41.04%) were airport staff, and 94 patients (44.34%) in 32 families were infected. There were 53 (25.00%) and 103 (48.58%) cases with one-dose and two-dose vaccination, respectively, and 55 (25.94%), 147 (69.34%) and 10 (4.72%) had mild, moderate and severe symptoms, respectively. The duration of viral shedding, or viral shedding time (VST), was significantly longer in unvaccinated individuals compared to vaccinated individuals (<i>p </i>=<i> </i>0.0008). Moreover, the duration was significantly longer in patients who received one vaccine dose than those who received two doses (<i>p </i><<i> </i>0.0001). The mild patients had significantly shorter VSTs than the moderate subjects (<i>p </i><<i> </i>0.0001). Disease severity and vaccination dose were independent predictors for VST by Cox regression models. Conclusions: These results suggest that two-dose vaccination could reduce VST in patients with the COVID-19 Delta variant. Chinese inactivated vaccines may decrease the disease severity of cases with the COVID-19 Delta variant.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=FuqunLiu" target="_blank"> Fuqun Liu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=ShufeiWu" target="_blank"> Shufei Wu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=MengyingLiu" target="_blank"> Mengying Liu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=LiliWang" target="_blank"> Lili Wang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=XinmeiHuang" target="_blank"> Xinmei Huang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=FuchaoLi" target="_blank"> Fuchao Li </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=WeihuaWu" target="_blank"> Weihua Wu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YingXu" target="_blank"> Ying Xu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=ZhigangZhao" target="_blank"> Zhigang Zhao </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YangyangXia" target="_blank"> Yangyang Xia </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YujuanWang" target="_blank"> Yujuan Wang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=YueYang" target="_blank"> Yue Yang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=WeiWang" target="_blank"> Wei Wang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=HaisenZhou" target="_blank"> Haisen Zhou* </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=MengshuCao" target="_blank"> Mengshu Cao* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/09/29/b95a88d6ab294c631c77c01a9f3fb3ca.png" data-lightbox="image-8" data-title=""><img src="/uploads/2024/09/29/b95a88d6ab294c631c77c01a9f3fb3ca.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Commentary</h4> <span>18 September 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/281">Primed Lung−Vagus−Brainstem Circuit by Allergen Triggers Airway Hyperactivity</a> </h3> <p class="article-abseract clamp">The nucleus of the solitary tract (NTS) is the primary hub for sensing and integrating respiratory information. It integrates input from the vagus and glossopharyngeal nerve. It interacts with other brainstem nuclei, such as the nucleus ambiguus (NA) and the dorsal motor nucleus of the vagus (DMV), to transmit information and initiate a neuroreflex response to respiratory stimuli. In a recent issue of the journal Nature, Su et al. demonstrated that <i>Dbh<sup>+</sup></i> neurons in the NTS can receive signals from vagal <i>Trpv1</i><sup>+</sup> sensory neurons that sense allergen−induced IL−4 production in mast cells and pass the signal to <i>Chat</i><sup>+</sup> neurons in the NA by releasing norepinephrine. Subsequently, NA <i>Chat</i><sup>+</sup> neurons drive allergen−induced airway hyperresponsiveness by projecting onto cholinergic pulmonary ganglia in the lungs. This study not only provides new insights into the regulation of allergen−induced airway hyperresponsiveness by lung−vagus<b>–</b>brainstem interoceptive circuit but also provides us with new strategies to combat asthma.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=RenlanWu" target="_blank"> Renlan Wu </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=JieChen" target="_blank"> Jie Chen </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=XiaoSu" target="_blank"> Xiao Su* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/09/18/283de03959932bfe08c3af6afc1509c0.jpg" data-lightbox="image-9" data-title=""><img src="/uploads/2024/09/18/283de03959932bfe08c3af6afc1509c0.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Editorial</h4> <span>13 September 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/278">Hypoxic Ventilatory Response in Highlander and Lowlander Chinese Patients with Sleep Apnea</a> </h3> <p class="article-abseract clamp">The aim of the study was to compare Hypoxic Ventilatory Response (HVR) of sleep apnea in Uygur patients stemming from higher altitude and Chinese Han patients from sea level. 276 subjects with or without snoring from the Karamay community were recruited. 226 subjects (<i>n</i> = 71 Han OSA patients, <i>n</i> = 75 Uygur OSA patients,<i> n</i> = 52 for Uygur control subjects without OSA, <i>n</i> = 28 Han control subjects without OSA) were matched for age and gender. All patients were assessed via polysomnography (PSG). Lung function was assessed. Apnea-hypopnea index (AHI), mean SaO<sub>2</sub> (MSaO<sub>2</sub>%), lowest SaO<sub>2</sub> (LSaO<sub>2</sub>%), the number of desaturations ≥4% per hour (ODI4), FEV1/FVC ratio, HVR, △VE/△SaO<sub>2</sub> and the pulse responses to hypoxia changes (ΔPulse/ΔSaO<sub>2</sub>) were calculated. A multiple logistic regression using a binary outcome for HVR was applied. (1) In control subjects without OSA, those living at high altitude (Uygur) had a lower HVR than control subjects living at sea level (Han) [−0.35L·min<sup>−1</sup> per %SpO<sub>2</sub>(−0.49 to−0.20 L·min<sup>−1</sup> per %SpO<sub>2</sub>) vs.−0.44 L·min<sup>−1</sup> per %SpO<sub>2</sub>(−0.55 to −0.21 L·min<sup>−1</sup> per %SpO<sub>2</sub>)]. (2) Compared to patients with OSA living at sea level (Han), those OSA patients living at high altitude (Uygur) had a higher neck circumference [43 cm (range 39<b>–</b>45 cm) vs. 42 cm (41<b>–</b>46) cm], higher abdominal circumference [110 cm (102<b>–</b>120 cm) vs. 101 cm (98<b>–</b>111 cm], higher LSaO<sub>2</sub> [81% (72<b>–</b>85%) vs. 76% (68<b>–</b>81%)], lower AHI [26 events/h (16<b>–</b>43 events/h) vs. 36 events/h (24<b>–</b>62 events/h)] and lower ODI4 [15/h (7<b>–</b>29/h) vs. 37/h (20<b>–</b>54/h)]. (3) Considering patients with mild OSA, those who lived at high altitude (Uygur) had a weaker HVR compared to Han patients [−0.31 L·min<sup>−1</sup> per %SpO<sub>2</sub>(−0.42 to −0.20 L·min<sup>−1</sup> per %SpO<sub>2</sub>) vs.−0.47 L·min<sup>−1</sup> per %SpO<sub>2</sub>(−0.59 to −0.21 L·min<sup>−1</sup> per %SpO<sub>2</sub>)]. However, in moderate and severe OSA the difference in HVR between people living at high and low altitudes was not significant. In people living at high altitude (Uygur) compared to sea level (Han), HVR is weaker both in control subjects and those with mild OSA, but this difference between populations living at different altitudes in those with moderate and severe OSA is not obvious.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Zhong-MingHe" target="_blank"> Zhong-Ming He </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Xue-LongJiang" target="_blank"> Xue-Long Jiang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Xiao-SongDong" target="_blank"> Xiao-Song Dong </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Qing-LongZhang" target="_blank"> Qing-Long Zhang </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=Mei-RongHan" target="_blank"> Mei-Rong Han </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=PiliqingDa" target="_blank"> Piliqing Da </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=FanHan" target="_blank"> Fan Han </a> </div> <div class="author-name"> <a href="https://scholar.google.com/scholar?q=ThomasPenzel" target="_blank"> Thomas Penzel* </a> </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/09/13/aefc4cb5bf8374a438895e83bb6eab3a.jpg" data-lightbox="image-10" data-title=""><img src="/uploads/2024/09/13/aefc4cb5bf8374a438895e83bb6eab3a.jpg" class=""></a> </div> </div> </div> </div> <div class="tab-pane fade" id="id-downloaded"> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>19 February 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/134">Single Cell Analysis of Lung Lymphatic Endothelial Cells and Lymphatic Responses during Influenza Infection</a> </h3> <p class="article-abseract clamp">Tissue lymphatic vessels network plays critical roles in immune surveillance and tissue homeostasis in response to pathogen invasion, but how lymphatic system <em>per se</em> is remolded during infection is less understood. Here, we observed that influenza infection induces a significant increase of lymphatic vessel numbers in the lung, accompanied with extensive proliferation of lymphatic endothelial cells (LECs). Single-cell RNA sequencing illustrated the heterogeneity of LECs, identifying a novel PD-L1<sup>+</sup> subpopulation that is present during viral infection but not at steady state. Specific deletion of <em>Pd-l1</em> in LECs elevated the expansion of lymphatic vessel numbers during viral infection. Together these findings elucidate a dramatic expansion of lung lymphatic network in response to viral infection, and reveal a PD-L1<sup>+</sup> LEC subpopulation that potentially modulates lymphatic vessel remolding.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> JianGe </div> <div class="author-name"> HongxiaShao </div> <div class="author-name"> HongxuDing </div> <div class="author-name"> YuefengHuang </div> <div class="author-name"> XuebingWu </div> <div class="author-name"> JieSun </div> <div class="author-name"> JianwenQue </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202402/20/21fceb390f9ea08ca16510ca86684301.jpg" data-lightbox="image-1" data-title=""><img src="/uploads/image/202402/20/21fceb390f9ea08ca16510ca86684301.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>30 April 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/181">Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis</a> </h3> <p class="article-abseract clamp">The molecular mechanisms that regulate progressive pulmonary fibrosis remain poorly understood. Type 2 alveolar epithelial cells (AEC2s) function as adult stem cells in the lung. We previously showed that there is a loss of AEC2s and a failure of AEC2 renewal in the lungs of idiopathic pulmonary fibrosis (IPF) patients.<span class="apple-converted-space"> </span>We also reported that beta-arrestins are the key regulators of fibroblast invasion, and beta-arrestin 1 and 2 deficient mice exhibit decreased mortality, decreased matrix deposition, and increased lung function in bleomycin-induced lung fibrosis. However, the role of beta-arrestins in AEC2 regeneration is unclear. In this study, we investigated the role and mechanism of Arrestin beta 1 (ARRB1) in AEC2 renewal and in lung fibrosis. We used conventional deletion as well as cell type-specific deletion of <i>ARRB1</i> in mice and found that <i>Arrb1</i> deficiency in fibroblasts protects mice from lung fibrosis, and the knockout mice exhibit enhanced AEC2 regeneration in vivo, suggesting a role of fibroblast-derived ARRB1 in AEC2 renewal. We further found that <i>Arrb1</i>-deficient fibroblasts promotes AEC2 renewal in 3D organoid assays. Mechanistically, we found that CCL7 is among the top downregulated cytokines in <i>Arrb1</i> deficient fibroblasts and CCL7 inhibits AEC2 regeneration in 3D organoid experiments. Therefore, fibroblast ARRB1 mediates AEC2 renewal, possibly by releasing chemokine CCL7, leading to fibrosis in the lung.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> GuanlingHuang </div> <div class="author-name"> YanGeng </div> <div class="author-name"> VrishikaKulur </div> <div class="author-name"> NingshanLiu </div> <div class="author-name"> XueLiu </div> <div class="author-name"> ForoughTaghavifar </div> <div class="author-name"> JiurongLiang </div> <div class="author-name"> PaulW.Noble </div> <div class="author-name"> DianhuaJiang </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202404/30/f2be5da53e024cc42a1663a2bc9c8866.jpg" data-lightbox="image-2" data-title=""><img src="/uploads/image/202404/30/f2be5da53e024cc42a1663a2bc9c8866.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>01 February 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/128">Molecular Regulation of Transforming Growth Factor-β1-induced Thioredoxin-interacting Protein Ubiquitination and Proteasomal Degradation in Lung Fibroblasts: Implication in Pulmonary Fibrosis</a> </h3> <p class="article-abseract clamp">Thioredoxin-interacting protein (TXNIP) plays a critical role in regulation of cellular redox reactions and inflammatory responses by interacting with thioredoxin (TRX) or the inflammasome. The role of TXNIP in lung fibrosis and molecular regulation of its stability have not been well studied. Therefore, here we investigated the molecular regulation of TXNIP stability and its role in TGF-β1-mediated signaling in lung fibroblasts. TXNIP protein levels were significantly decreased in lung tissues from bleomycin-challenged mice. Overexpression of TXNIP attenuated transforming growth factor-β1 (TGF-β1)-induced phosphorylation of Smad2/3 and fibronectin expression in lung fibroblasts, suggesting that decrease in TXNIP may contribute to the pathogenesis of lung fibrosis. Further, we observed that TGF-β1 lowered TXNIP protein levels, while TXNIP mRNA levels were unaltered by TGF-β1 exposure. TGF-β1 induced TXNIP degradation via the ubiquitin-proteasome system. A serine residue mutant (TNXIP-S308A) was resistant to TGF-β1-induced degradation. Furthermore, downregulation of ubiquitin-specific protease-13 (USP13) promoted the TGF-β1-induced TXNIP ubiquitination and degradation. Mechanistic studies revealed that USP13 targeted and deubiquitinated TXNIP. The results of this study revealed that the decrease of TXNIP in lungs apparently contributes to the pathogenesis of pulmonary fibrosis and that USP13 can target TXNP for deubiquitination and regulate its stability.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> SarahJTaleb </div> <div class="author-name"> QinmaoYe </div> <div class="author-name"> BoinaBaoyinna </div> <div class="author-name"> MichaelDedad </div> <div class="author-name"> DakshinPisini </div> <div class="author-name"> NarasimhamLParinandi </div> <div class="author-name"> LewisCCantley </div> <div class="author-name"> JingZhao </div> <div class="author-name"> YutongZhao </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202402/20/b54b2f7441eb9817bfba510da5211956.png" data-lightbox="image-3" data-title=""><img src="/uploads/image/202402/20/b54b2f7441eb9817bfba510da5211956.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>31 March 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/157"><p> The Asthma Risk Gene, <em>GSDMB</em>, Promotes Mitochondrial DNA-induced <em>ISGs</em> Expression </p></a> </h3> <p class="article-abseract clamp">Released mitochondrial DNA (mtDNA) in cells activates cGAS-STING pathway, which induces expression of interferon-stimulated genes (ISGs) and thereby promotes inflammation, as frequently seen in asthmatic airways. However, whether the genetic determinant, Gasdermin B (GSDMB), the most replicated asthma risk gene, regulates this pathway remains unknown.<b> </b>We set out to determine whether and how GSDMB regulates mtDNA-activated cGAS-STING pathway and subsequent <i>ISGs </i>induction in human airway epithelial cells. Using qPCR, ELISA, native polyacrylamide gel electrophoresis, co-immunoprecipitation and immunofluorescence assays, we evaluated the regulation of GSDMB on cGAS-STING pathway in both BEAS-2B cells and primary normal human bronchial epithelial cells (nHBEs). mtDNA was extracted in plasma samples from human asthmatics and the correlation between mtDNA levels and eosinophil counts was analyzed. <i>GSDMB </i>is significantly associated with <i>RANTES </i>expression in asthmatic nasal epithelial brushing samples from the Genes-environments and Admixture in Latino Americans (GALA) II study. Over-expression of <i>GSDMB</i> promotes DNA-induced IFN and <i>ISGs expression</i> in bronchial epithelial BEAS-2B cells and nHBEs. Conversely, knockout of <i>GSDMB </i>led to weakened induction of <i>interferon </i>(IFNs) and <i>ISGs</i> in BEAS-2B cells. Mechanistically, GSDMB interacts with the C-terminus of STING, promoting the translocalization of STING to Golgi, leading to the phosphorylation of IRF3 and induction of <i>IFNs </i>and <i>ISGs</i>. mtDNA copy number in serum from asthmatics was significantly correlated with blood eosinophil counts especially in male subjects. GSDMB promotes the activation of mtDNA and poly (dA:dT)-induced activation of cGAS-STING pathway in airway epithelial cells, leading to enhanced induction of <i>ISGs.</i><i></i></p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> TaoLiu </div> <div class="author-name"> Julian Hecker </div> <div class="author-name"> SiqiLiu </div> <div class="author-name"> XianliangRui </div> <div class="author-name"> Nathan Boyer </div> <div class="author-name"> Jennifer Wang </div> <div class="author-name"> Yuzhen Yu </div> <div class="author-name"> YihanZhang </div> <div class="author-name"> Hongmei Mou </div> <div class="author-name"> Luis Guillermo Gomez-Escobar </div> <div class="author-name"> Augustine M.K.Choi </div> <div class="author-name"> Benjamin A.Raby </div> <div class="author-name"> Scott T.Weiss </div> <div class="author-name"> Xiaobo Zhou </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202404/07/ede2d2a132fbda835b5d5d27fd325a5d.png" data-lightbox="image-4" data-title=""><img src="/uploads/image/202404/07/ede2d2a132fbda835b5d5d27fd325a5d.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Editorial</h4> <span>21 November 2023</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/88">The Journal of Respiratory Biology and Translational Medicine, a Versatile Platform for Basic and Clinical Science</a> </h3> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> Jeffrey A. Whitsett </div> <div class="author-name"> Jianwen Que </div> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>28 March 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/156">Glutamine Metabolism Is Required for Alveolar Macrophage Proliferation</a> </h3> <p class="article-abseract clamp">Alveolar macrophages (AMs) are critical for normal lung homeostasis, surfactant metabolism, and host defense against various respiratory pathogens. Despite being terminally differentiated cells, AMs are able to proliferate and self-renew to maintain their compartment without the input of the hematopoietic system in the adulthood during homeostasis. However, the molecular and metabolic mechanisms modulating AM proliferative responses are still incompletely understood. Here we have investigated the metabolic regulation of AM proliferation and self-renewal. Inhibition of glucose uptake or fatty acid oxidation did not significantly impact AM proliferation. Rather, inhibition of the glutamine uptake and/or glutaminase activity impaired AM mitochondrial respiration and cellular proliferation in vitro and in vivo in response to growth factor stimulation. Furthermore, mice with a genetic deletion of glutaminase in macrophages showed decreased proliferation. Our data indicate that glutamine is a critical substrate for fueling mitochondrial metabolism that is required for AM proliferation. Overall, our study is expected to shed light on the AM maintenance and repopulation by glutamine during homeostasis and following acute respiratory viral infection.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> MinWang </div> <div class="author-name"> BiboZhu </div> <div class="author-name"> ChengZhang </div> <div class="author-name"> ChaofanLi </div> <div class="author-name"> Ruixuan Zhang </div> <div class="author-name"> JefferyC.Rathmell </div> <div class="author-name"> HuLi </div> <div class="author-name"> WeiguoCui </div> <div class="author-name"> Taro Hitosugi </div> <div class="author-name"> JieSun </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/03/28/15685de68e323ba2aa5607ae78f1c4ef.png" data-lightbox="image-6" data-title=""><img src="/uploads/2024/03/28/15685de68e323ba2aa5607ae78f1c4ef.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Commentary</h4> <span>17 June 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/214">Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus</a> </h3> <p class="article-abseract clamp">The ubiquitin system has been shown to play an important role in regulation of immune responses during viral infection. In a recent article published in Science Signaling, Wu and colleagues revealed that transcriptional factor Miz1 plays a pro-viral role in influenza A virus (IAV) infection by suppressing type I interferons (IFNs) production through recruiting HDAC1 to ifnb1 promoter. They show that a series of E3 ligases combinatorially regulates Miz1 ubiquitination and degradation and modulates IFNs production and viral replication.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> BoyuXia </div> <div class="author-name"> JingZhao </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/06/17/0e22fe71a584312daac2cc6a6b2e1723.png" data-lightbox="image-7" data-title=""><img src="/uploads/2024/06/17/0e22fe71a584312daac2cc6a6b2e1723.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Communication</h4> <span>30 May 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/196">A Novel Animal Model for Pulmonary Hypertension: Lung Endothelial-Specific Deletion of <em>Egln1</em> in Mice</a> </h3> <p class="article-abseract clamp">Pulmonary arterial hypertension (PAH) is a devastating disease characterized by high blood pressure in the pulmonary arteries, which can potentially lead to heart failure over time. Previously, our lab found that endothelia-specific knockout of <i>Egln1</i>, encoding prolyl 4-hydroxylase-2 (PHD2), induced spontaneous pulmonary hypertension (PH). Recently, we elucidated that <i>Tmem100</i> is a lung-specific endothelial gene using <i>Tmem100-CreERT2</i> mice. We hypothesize that lung endothelial-specific deletion of <i>Egln1</i> could lead to the development of PH without affecting<i> Egln1</i> gene expression in other organs. <i>Tm</i>em<i>100</i>-CreERT2 mice were crossed with <i>Egln1<sup>flox/flox</sup> </i>mice to generate <i>Egln1<sup>f/f</sup>;Tmem100-CreERT2 </i>(LiCKO) mice. Western blot and immunofluorescent staining were performed to verify the knockout efficacy of <i>Egln1</i> in multiple organs of LiCKO mice. PH phenotypes, including hemodynamics, right heart size and function, pulmonary vascular remodeling, were evaluated by right heart catheterization and echocardiography measurements. Tamoxifen treatment induced <i>Egln1</i> deletion in the lung endothelial cells (ECs) but not in other organs of adult LiCKO mice. LiCKO mice exhibited an increase in right ventricular systolic pressure (RVSP, ~35 mmHg) and right heart hypertrophy. Echocardiography measurements showed right heart hypertrophy, as well as cardiac and pulmonary arterial dysfunction. Pulmonary vascular remodeling, including increased pulmonary wall thickness and muscularization of distal pulmonary arterials, was enhanced in LiCKO mice compared to wild-type mice. <i>Tmem100</i> promoter-mediated lung endothelial knockout of <i>Egln1 </i>in mice leads to development of spontaneous PH. LiCKO mice could serve as a novel mouse model for PH to study lung and other organ crosstalk.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> BinLiu </div> <div class="author-name"> DanYi </div> <div class="author-name"> XiaokuangMa </div> <div class="author-name"> KarinaRamirez </div> <div class="author-name"> HanqiuZhao </div> <div class="author-name"> XiaomeiXia </div> <div class="author-name"> MichaelB.Fallon </div> <div class="author-name"> VladimirV.Kalinichenko </div> <div class="author-name"> ShenfengQiu </div> <div class="author-name"> ZhiyuDai </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202405/31/199d97621ab33294dab275410d118a5c.png" data-lightbox="image-8" data-title=""><img src="/uploads/image/202405/31/199d97621ab33294dab275410d118a5c.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Commentary</h4> <span>12 June 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/210">Dual Genetic Tracing Reveals the Origin of Alveolar Stem Cells after Lung Injury</a> </h3> <p class="article-abseract clamp">As alveolar epithelial stem cells, alveolar type II (AT2) cells play a pivotal role in sustaining alveolar homeostasis and facilitating repair processes. However, the sources of AT2 cell regeneration have remained contentious due to the non-specific labeling limitations of traditional single recombinase-based lineage tracing techniques. To address this issue, we employed dual recombination systems to develop more precise lineage tracing methodologies, effectively bypassing the shortcomings of conventional approaches and enabling specific labeling of lung epithelial cells. Our findings demonstrate that, following lung injury, regenerated AT2 cells do not originate from alveolar type I (AT1) cells, but instead derive from bronchiolar club cells and bronchioalveolar stem cells (BASCs), alongside the self-renewal of resident AT2 cells. Furthermore, we discovered that the transition of club cells and BASCs into AT2 cells is distinctly modulated by the Notch signaling pathway. This study not only provides novel insights into lung regeneration, but the innovative lineage tracing technology developed herein also holds promise as a technical support for research in diverse fields.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> KuoLiu </div> <div class="author-name"> BinZhou </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/06/13/1dd075f3b4d300b112f7f20c2cc36a6c.png" data-lightbox="image-9" data-title=""><img src="/uploads/2024/06/13/1dd075f3b4d300b112f7f20c2cc36a6c.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>22 July 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/235">Aging-Associated Molecular Changes in Human Alveolar Type I Cells</a> </h3> <p class="article-abseract clamp">Human alveolar type I (AT1) cells are specialized epithelial cells that line the alveoli in the lungs where gas exchange occurs. The primary function of AT1 cells is not only to facilitate efficient gas exchange between the air and the blood in the lungs, but also to contribute to the structural integrity of the alveoli to maintain lung function and homeostasis. Aging has notable effects on the structure, function, and regenerative capacity of human AT1 cells. However, our understanding of the molecular mechanisms driving these age-related changes in AT1 cells remains limited. Leveraging a recent single-cell transcriptomics dataset we generated on healthy human lungs, we identified a series of significant molecular alterations in AT1 cells from aged lungs. Notably, the aged AT1 cells exhibited increased cellular senescence and chemokine gene expression, alongside diminished epithelial features such as decreases in cell junctions, endocytosis, and pulmonary matrisome gene expression. Gene set analyses also indicated that aged AT1 cells were resistant to apoptosis, a crucial mechanism for turnover and renewal of AT1 cells, thereby ensuring alveolar integrity and function. Further research on these alterations is imperative to fully elucidate the impact on AT1 cells and is indispensable for developing effective therapies to preserve lung function and promote healthy aging.</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> XueLiu </div> <div class="author-name"> XuexiZhang </div> <div class="author-name"> JiurongLiang </div> <div class="author-name"> PaulW.Noble </div> <div class="author-name"> DianhuaJiang </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202407/22/efb6d52eaec3168dbf84a9a26b53559f.jpg" data-lightbox="image-10" data-title=""><img src="/uploads/image/202407/22/efb6d52eaec3168dbf84a9a26b53559f.jpg" class=""></a> </div> </div> </div> </div> <div class="tab-pane fade" id="id-popular"> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>31 March 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/157"><p> The Asthma Risk Gene, <em>GSDMB</em>, Promotes Mitochondrial DNA-induced <em>ISGs</em> Expression </p></a> </h3> <p class="article-abseract clamp"> Released mitochondrial DNA (mtDNA) in cells activates cGAS-STING pathway, which induces expression of interferon-stimulated genes (ISGs) and thereby promotes inflammation, as frequently seen in asthmatic airways. However, whether the genetic determinant, Gasdermin B (GSDMB), the most replicated asthma risk gene, regulates this pathway remains unknown.<b> </b>We set out to determine whether and how GSDMB regulates mtDNA-activated cGAS-STING pathway and subsequent <i>ISGs </i>induction in human airway epithelial cells. Using qPCR, ELISA, native polyacrylamide gel electrophoresis, co-immunoprecipitation and immunofluorescence assays, we evaluated the regulation of GSDMB on cGAS-STING pathway in both BEAS-2B cells and primary normal human bronchial epithelial cells (nHBEs). mtDNA was extracted in plasma samples from human asthmatics and the correlation between mtDNA levels and eosinophil counts was analyzed. <i>GSDMB </i>is significantly associated with <i>RANTES </i>expression in asthmatic nasal epithelial brushing samples from the Genes-environments and Admixture in Latino Americans (GALA) II study. Over-expression of <i>GSDMB</i> promotes DNA-induced IFN and <i>ISGs expression</i> in bronchial epithelial BEAS-2B cells and nHBEs. Conversely, knockout of <i>GSDMB </i>led to weakened induction of <i>interferon </i>(IFNs) and <i>ISGs</i> in BEAS-2B cells. Mechanistically, GSDMB interacts with the C-terminus of STING, promoting the translocalization of STING to Golgi, leading to the phosphorylation of IRF3 and induction of <i>IFNs </i>and <i>ISGs</i>. mtDNA copy number in serum from asthmatics was significantly correlated with blood eosinophil counts especially in male subjects. GSDMB promotes the activation of mtDNA and poly (dA:dT)-induced activation of cGAS-STING pathway in airway epithelial cells, leading to enhanced induction of <i>ISGs.</i><i></i>utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> TaoLiu </div> <div class="author-name"> Julian Hecker </div> <div class="author-name"> SiqiLiu </div> <div class="author-name"> XianliangRui </div> <div class="author-name"> Nathan Boyer </div> <div class="author-name"> Jennifer Wang </div> <div class="author-name"> Yuzhen Yu </div> <div class="author-name"> YihanZhang </div> <div class="author-name"> Hongmei Mou </div> <div class="author-name"> Luis Guillermo Gomez-Escobar </div> <div class="author-name"> Augustine M.K.Choi </div> <div class="author-name"> Benjamin A.Raby </div> <div class="author-name"> Scott T.Weiss </div> <div class="author-name"> Xiaobo Zhou </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202404/07/ede2d2a132fbda835b5d5d27fd325a5d.png" data-lightbox="image-1" data-title=""><img src="/uploads/image/202404/07/ede2d2a132fbda835b5d5d27fd325a5d.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>01 February 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/128">Molecular Regulation of Transforming Growth Factor-β1-induced Thioredoxin-interacting Protein Ubiquitination and Proteasomal Degradation in Lung Fibroblasts: Implication in Pulmonary Fibrosis</a> </h3> <p class="article-abseract clamp"> Thioredoxin-interacting protein (TXNIP) plays a critical role in regulation of cellular redox reactions and inflammatory responses by interacting with thioredoxin (TRX) or the inflammasome. The role of TXNIP in lung fibrosis and molecular regulation of its stability have not been well studied. Therefore, here we investigated the molecular regulation of TXNIP stability and its role in TGF-β1-mediated signaling in lung fibroblasts. TXNIP protein levels were significantly decreased in lung tissues from bleomycin-challenged mice. Overexpression of TXNIP attenuated transforming growth factor-β1 (TGF-β1)-induced phosphorylation of Smad2/3 and fibronectin expression in lung fibroblasts, suggesting that decrease in TXNIP may contribute to the pathogenesis of lung fibrosis. Further, we observed that TGF-β1 lowered TXNIP protein levels, while TXNIP mRNA levels were unaltered by TGF-β1 exposure. TGF-β1 induced TXNIP degradation via the ubiquitin-proteasome system. A serine residue mutant (TNXIP-S308A) was resistant to TGF-β1-induced degradation. Furthermore, downregulation of ubiquitin-specific protease-13 (USP13) promoted the TGF-β1-induced TXNIP ubiquitination and degradation. Mechanistic studies revealed that USP13 targeted and deubiquitinated TXNIP. The results of this study revealed that the decrease of TXNIP in lungs apparently contributes to the pathogenesis of pulmonary fibrosis and that USP13 can target TXNP for deubiquitination and regulate its stability.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> SarahJTaleb </div> <div class="author-name"> QinmaoYe </div> <div class="author-name"> BoinaBaoyinna </div> <div class="author-name"> MichaelDedad </div> <div class="author-name"> DakshinPisini </div> <div class="author-name"> NarasimhamLParinandi </div> <div class="author-name"> LewisCCantley </div> <div class="author-name"> JingZhao </div> <div class="author-name"> YutongZhao </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202402/20/b54b2f7441eb9817bfba510da5211956.png" data-lightbox="image-2" data-title=""><img src="/uploads/image/202402/20/b54b2f7441eb9817bfba510da5211956.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>19 February 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/134">Single Cell Analysis of Lung Lymphatic Endothelial Cells and Lymphatic Responses during Influenza Infection</a> </h3> <p class="article-abseract clamp"> Tissue lymphatic vessels network plays critical roles in immune surveillance and tissue homeostasis in response to pathogen invasion, but how lymphatic system <em>per se</em> is remolded during infection is less understood. Here, we observed that influenza infection induces a significant increase of lymphatic vessel numbers in the lung, accompanied with extensive proliferation of lymphatic endothelial cells (LECs). Single-cell RNA sequencing illustrated the heterogeneity of LECs, identifying a novel PD-L1<sup>+</sup> subpopulation that is present during viral infection but not at steady state. Specific deletion of <em>Pd-l1</em> in LECs elevated the expansion of lymphatic vessel numbers during viral infection. Together these findings elucidate a dramatic expansion of lung lymphatic network in response to viral infection, and reveal a PD-L1<sup>+</sup> LEC subpopulation that potentially modulates lymphatic vessel remolding.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> JianGe </div> <div class="author-name"> HongxiaShao </div> <div class="author-name"> HongxuDing </div> <div class="author-name"> YuefengHuang </div> <div class="author-name"> XuebingWu </div> <div class="author-name"> JieSun </div> <div class="author-name"> JianwenQue </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202402/20/21fceb390f9ea08ca16510ca86684301.jpg" data-lightbox="image-3" data-title=""><img src="/uploads/image/202402/20/21fceb390f9ea08ca16510ca86684301.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>30 April 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/181">Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis</a> </h3> <p class="article-abseract clamp"> The molecular mechanisms that regulate progressive pulmonary fibrosis remain poorly understood. Type 2 alveolar epithelial cells (AEC2s) function as adult stem cells in the lung. We previously showed that there is a loss of AEC2s and a failure of AEC2 renewal in the lungs of idiopathic pulmonary fibrosis (IPF) patients.<span class="apple-converted-space"> </span>We also reported that beta-arrestins are the key regulators of fibroblast invasion, and beta-arrestin 1 and 2 deficient mice exhibit decreased mortality, decreased matrix deposition, and increased lung function in bleomycin-induced lung fibrosis. However, the role of beta-arrestins in AEC2 regeneration is unclear. In this study, we investigated the role and mechanism of Arrestin beta 1 (ARRB1) in AEC2 renewal and in lung fibrosis. We used conventional deletion as well as cell type-specific deletion of <i>ARRB1</i> in mice and found that <i>Arrb1</i> deficiency in fibroblasts protects mice from lung fibrosis, and the knockout mice exhibit enhanced AEC2 regeneration in vivo, suggesting a role of fibroblast-derived ARRB1 in AEC2 renewal. We further found that <i>Arrb1</i>-deficient fibroblasts promotes AEC2 renewal in 3D organoid assays. Mechanistically, we found that CCL7 is among the top downregulated cytokines in <i>Arrb1</i> deficient fibroblasts and CCL7 inhibits AEC2 regeneration in 3D organoid experiments. Therefore, fibroblast ARRB1 mediates AEC2 renewal, possibly by releasing chemokine CCL7, leading to fibrosis in the lung.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> GuanlingHuang </div> <div class="author-name"> YanGeng </div> <div class="author-name"> VrishikaKulur </div> <div class="author-name"> NingshanLiu </div> <div class="author-name"> XueLiu </div> <div class="author-name"> ForoughTaghavifar </div> <div class="author-name"> JiurongLiang </div> <div class="author-name"> PaulW.Noble </div> <div class="author-name"> DianhuaJiang </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202404/30/f2be5da53e024cc42a1663a2bc9c8866.jpg" data-lightbox="image-4" data-title=""><img src="/uploads/image/202404/30/f2be5da53e024cc42a1663a2bc9c8866.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Communication</h4> <span>30 May 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/196">A Novel Animal Model for Pulmonary Hypertension: Lung Endothelial-Specific Deletion of <em>Egln1</em> in Mice</a> </h3> <p class="article-abseract clamp"> Pulmonary arterial hypertension (PAH) is a devastating disease characterized by high blood pressure in the pulmonary arteries, which can potentially lead to heart failure over time. Previously, our lab found that endothelia-specific knockout of <i>Egln1</i>, encoding prolyl 4-hydroxylase-2 (PHD2), induced spontaneous pulmonary hypertension (PH). Recently, we elucidated that <i>Tmem100</i> is a lung-specific endothelial gene using <i>Tmem100-CreERT2</i> mice. We hypothesize that lung endothelial-specific deletion of <i>Egln1</i> could lead to the development of PH without affecting<i> Egln1</i> gene expression in other organs. <i>Tm</i>em<i>100</i>-CreERT2 mice were crossed with <i>Egln1<sup>flox/flox</sup> </i>mice to generate <i>Egln1<sup>f/f</sup>;Tmem100-CreERT2 </i>(LiCKO) mice. Western blot and immunofluorescent staining were performed to verify the knockout efficacy of <i>Egln1</i> in multiple organs of LiCKO mice. PH phenotypes, including hemodynamics, right heart size and function, pulmonary vascular remodeling, were evaluated by right heart catheterization and echocardiography measurements. Tamoxifen treatment induced <i>Egln1</i> deletion in the lung endothelial cells (ECs) but not in other organs of adult LiCKO mice. LiCKO mice exhibited an increase in right ventricular systolic pressure (RVSP, ~35 mmHg) and right heart hypertrophy. Echocardiography measurements showed right heart hypertrophy, as well as cardiac and pulmonary arterial dysfunction. Pulmonary vascular remodeling, including increased pulmonary wall thickness and muscularization of distal pulmonary arterials, was enhanced in LiCKO mice compared to wild-type mice. <i>Tmem100</i> promoter-mediated lung endothelial knockout of <i>Egln1 </i>in mice leads to development of spontaneous PH. LiCKO mice could serve as a novel mouse model for PH to study lung and other organ crosstalk.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> BinLiu </div> <div class="author-name"> DanYi </div> <div class="author-name"> XiaokuangMa </div> <div class="author-name"> KarinaRamirez </div> <div class="author-name"> HanqiuZhao </div> <div class="author-name"> XiaomeiXia </div> <div class="author-name"> MichaelB.Fallon </div> <div class="author-name"> VladimirV.Kalinichenko </div> <div class="author-name"> ShenfengQiu </div> <div class="author-name"> ZhiyuDai </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202405/31/199d97621ab33294dab275410d118a5c.png" data-lightbox="image-5" data-title=""><img src="/uploads/image/202405/31/199d97621ab33294dab275410d118a5c.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>28 March 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/156">Glutamine Metabolism Is Required for Alveolar Macrophage Proliferation</a> </h3> <p class="article-abseract clamp"> Alveolar macrophages (AMs) are critical for normal lung homeostasis, surfactant metabolism, and host defense against various respiratory pathogens. Despite being terminally differentiated cells, AMs are able to proliferate and self-renew to maintain their compartment without the input of the hematopoietic system in the adulthood during homeostasis. However, the molecular and metabolic mechanisms modulating AM proliferative responses are still incompletely understood. Here we have investigated the metabolic regulation of AM proliferation and self-renewal. Inhibition of glucose uptake or fatty acid oxidation did not significantly impact AM proliferation. Rather, inhibition of the glutamine uptake and/or glutaminase activity impaired AM mitochondrial respiration and cellular proliferation in vitro and in vivo in response to growth factor stimulation. Furthermore, mice with a genetic deletion of glutaminase in macrophages showed decreased proliferation. Our data indicate that glutamine is a critical substrate for fueling mitochondrial metabolism that is required for AM proliferation. Overall, our study is expected to shed light on the AM maintenance and repopulation by glutamine during homeostasis and following acute respiratory viral infection.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> MinWang </div> <div class="author-name"> BiboZhu </div> <div class="author-name"> ChengZhang </div> <div class="author-name"> ChaofanLi </div> <div class="author-name"> Ruixuan Zhang </div> <div class="author-name"> JefferyC.Rathmell </div> <div class="author-name"> HuLi </div> <div class="author-name"> WeiguoCui </div> <div class="author-name"> Taro Hitosugi </div> <div class="author-name"> JieSun </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/03/28/15685de68e323ba2aa5607ae78f1c4ef.png" data-lightbox="image-6" data-title=""><img src="/uploads/2024/03/28/15685de68e323ba2aa5607ae78f1c4ef.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>11 October 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/300">Surfactant Protein-C Regulates Alveolar Type 2 Epithelial Cell Lineages via the CD74 Receptor</a> </h3> <p class="article-abseract clamp"> Deficiency of surfactant protein-C (SPC) increases susceptibility to lung infections and injury, and suppressed expression of SPC has been associated with the severity of acute respiratory distress syndrome (ARDS). Alveolar type 2 epithelial cells (AT2) are critical for maintenance and repair of the lung. However, the role of the SPC in the regulation of AT2 cell lineage and the underlying mechanisms are not completely understood. This study aimed to investigate the mechanisms by which SPC regulates AT2 lineages. <i>Sftpc−/− </i>mice were used to model the SPC deficiency in ARDS patients. We utilized three-dimensional (3D) organoids to compare AT2 lineage characteristics between wild type (WT) and <i>Sftpc−/− </i>mice by analyzing AT2 proliferation, alveolar type 1 cells (AT1) differentiation and CD74 expression, using colony-formation assay, immunofluorescence, flow cytometry, and immunoblots. The results showed that <i>Sftpc</i>−/− mice demonstrated a reduced AT2 cell population. Influenza A virus subtype H1N1 (H1N1) infected <i>Sftpc−/− </i>mice demonstrated reduced AT2 proliferation and AT1 differentiation. Western blot indicated elevated levels of CD74 protein in AT2 cells of <i>Sftpc−/− </i>mice. Colony-forming efficiency was significantly attenuated in AT2 cells isolated from <i>Sftpc−/− </i>mice compared to the WT controls. Podoplanin (PDPN, a marker of AT1 cells) expression and transient cell count significantly increased in <i>Sftpc−/− </i>organoids. Moreover, siRNA-mediated gene silencing of CD74 in AT2 cells significantly increased AT2 proliferation and AT1 differentiation in <i>Sftpc−/− </i>organoids. This study suggests that SPC regulates AT2 lineage in vitro and in vivo. The SPC might influence AT2 lineage during the lung epithelium repair by activating signaling mechanism involving CD74 receptor.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> KrishanG.Jain </div> <div class="author-name"> YangLiu </div> <div class="author-name"> RunzhenZhao </div> <div class="author-name"> PreetiJ.Muire </div> <div class="author-name"> Nan-Miles Xi </div> <div class="author-name"> Hong-LongJi </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/10/11/5e8caa6a23316115d46d6ec32df71303.jpg" data-lightbox="image-7" data-title=""><img src="/uploads/2024/10/11/5e8caa6a23316115d46d6ec32df71303.jpg" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Review</h4> <span>25 June 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/221">Solute Carrier Family 26 Member 4 (SLC26A4), A Potential Therapeutic Target for Asthma</a> </h3> <p class="article-abseract clamp"> Asthma is a prevalent respiratory condition with multifaceted pathomechanisms, presenting challenges for therapeutic development. The SLC (Solute Carrier) gene family, encompassing diverse membrane transport proteins, plays pivotal roles in various human diseases by facilitating solute movement across biological membranes. These solutes include ions, sugars, amino acids, neurotransmitters, and drugs. Mutations in these ion channels have been associated with numerous disorders, underscoring the significance of SLC gene families in physiological processes. Among these, the SLC26A4 gene encodes pendrin, an anion exchange protein involved in transmembrane transport of chloride, iodide, and bicarbonate. Mutations in SLC26A4 are associated with Pendred syndrome. Elevated SLC26A4 expression has been linked to airway inflammation, hyperreactivity, and mucus production in asthma. Here, we review novel insights from SLC gene family members into the mechanisms of substrate transport and disease associations, with specific emphasis on SLC26A4. We explore triggers inducing SLC26A4 expression and its contributions to the pathogenesis of pulmonary diseases, particularly asthma. We summarize the inhibitors of SLC26A4 that have shown promise in the treatment of different phenotypes of diseases. While SLC26A4 inhibitors present potential treatments for asthma, further research is imperative to delineate their precise role in asthma pathogenesis and develop efficacious therapeutic strategies targeting this protein.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> Vineeta Guntupalli </div> <div class="author-name"> RongjunWan </div> <div class="author-name"> LiyuanLiu </div> <div class="author-name"> WenjingGu </div> <div class="author-name"> ShaobingXie </div> <div class="author-name"> PeisongGao </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/2024/06/25/cb30475956f886fce37a0bb25aaba23d.png" data-lightbox="image-8" data-title=""><img src="/uploads/2024/06/25/cb30475956f886fce37a0bb25aaba23d.png" class=""></a> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Editorial</h4> <span>21 November 2023</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/88">The Journal of Respiratory Biology and Translational Medicine, a Versatile Platform for Basic and Clinical Science</a> </h3> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> Jeffrey A. Whitsett </div> <div class="author-name"> Jianwen Que </div> </div> </div> </div> <div class="d-flex article-box pt-3 pb-3"> <div class="sc-width-200 pr-3"> <h4>Article</h4> <span>22 July 2024</span> </div> <div class="sc-flex-value1 d-flex flex-wrap"> <div> <h3 class="article-title"> <a class="anchor" href="/article/pii/235">Aging-Associated Molecular Changes in Human Alveolar Type I Cells</a> </h3> <p class="article-abseract clamp"> Human alveolar type I (AT1) cells are specialized epithelial cells that line the alveoli in the lungs where gas exchange occurs. The primary function of AT1 cells is not only to facilitate efficient gas exchange between the air and the blood in the lungs, but also to contribute to the structural integrity of the alveoli to maintain lung function and homeostasis. Aging has notable effects on the structure, function, and regenerative capacity of human AT1 cells. However, our understanding of the molecular mechanisms driving these age-related changes in AT1 cells remains limited. Leveraging a recent single-cell transcriptomics dataset we generated on healthy human lungs, we identified a series of significant molecular alterations in AT1 cells from aged lungs. Notably, the aged AT1 cells exhibited increased cellular senescence and chemokine gene expression, alongside diminished epithelial features such as decreases in cell junctions, endocytosis, and pulmonary matrisome gene expression. Gene set analyses also indicated that aged AT1 cells were resistant to apoptosis, a crucial mechanism for turnover and renewal of AT1 cells, thereby ensuring alveolar integrity and function. Further research on these alterations is imperative to fully elucidate the impact on AT1 cells and is indispensable for developing effective therapies to preserve lung function and promote healthy aging.utf-8</p> </div> <div class="authors-list align-self-end"> <i class="fal fa-user"></i> <div class="author-name"> XueLiu </div> <div class="author-name"> XuexiZhang </div> <div class="author-name"> JiurongLiang </div> <div class="author-name"> PaulW.Noble </div> <div class="author-name"> DianhuaJiang </div> </div> </div> <div class="article-img"> <div class="img-thumbnail"> <a href="/uploads/image/202407/22/efb6d52eaec3168dbf84a9a26b53559f.jpg" data-lightbox="image-10" data-title=""><img src="/uploads/image/202407/22/efb6d52eaec3168dbf84a9a26b53559f.jpg" class=""></a> </div> </div> </div> </div> </div> </div> </section> <section id="recent-posts-4" class="widget widget_recent_entries news-card mb-2"> <div class="my-body-container padding0"> <div class="section-heading"> <h3 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