AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 发表的论文报告了肺生物学领域的重要和原创性观察结果。该杂志的重点包括但不限于肺细胞和分子的细胞、生化、分子、发育、遗传和免疫学研究。

The American Journal of Respiratory Cell and Molecular Biology publishes significant and original research findings in the field of pulmonary biology. The journal focuses on various aspects including cellular, biochemical, molecular, developmental, genetic, and immunological studies of lung cells and molecules.

《American Journal of Respiratory Cell and Molecular Biology》发表肺生物学领域的重要原创研究成果。该杂志的重点包括肺细胞和分子的细胞生物学、生物化学、分子生物学、发育生物学、遗传学和免疫学研究等多个方面。

American Journal of Respiratory Cell and Molecular Biology

Neutrophil migration into infected tissues is essential for host defense, but products of activated neutrophils can be quite damaging to host cells. Neutrophil influx into the lung and airways and resultant inflammation characterizes diseases such as chronic obstructive pulmonary disease, bronchiectasis, and cystic fibrosis. To migrate, neutrophils must reorganize the actin cytoskeleton to establish a leading edge pseudopod and a trailing edge uropod. The actin-binding protein myristoylated alanine-rich C-kinase substrate (MARCKS) has been shown to bind and cross-link actin in a variety of cell types and to co-localize with F-actin in the leading edge lamellipodium of migrating fibroblasts. The hypothesis that MARCKS has a role in the regulation of neutrophil migration was tested using a cell-permeant peptide derived from the MARCKS myristoylated aminoterminus (MANS peptide). Treatment of isolated human neutrophils with MANS significantly inhibited both their migration and beta2 integrin-dependent adhesion in response to N-formyl-methionyl-leucyl-phenylalanine (fMLF), IL-8, or leukotriene (LT)B(4). The IC(50) for fMLF-induced migration and adhesion was 17.1 microM and 12.5 microM, respectively. MANS significantly reduced the F-actin content in neutrophils 30 seconds after fMLF stimulation, although the peptide did not alter the ability of cells to polarize or spread. MANS did not alter fMLF-induced increases in surface beta2 integrin expression. These results suggest that MARCKS, via its myristoylated aminoterminus, is a key regulator of neutrophil migration and adhesion.

Rachael E. Eckert

Laura E. Neuder

Joungjoa Park

Kenneth B. Adler

Samuel L. Jones

Am J Respir Cell Mol Biol

Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Protein Regulation of Human Neutrophil Migration

1. World Health Organization. Coronavirus disease (COVID-2019) situation reports. 2020 [accessed 2020 Aug 6]. Available from: https:// www.who.int/emergencies/diseases/novel-coronavirus-2019/ situation-reports. 2. Poston JT, Patel BK, Davis AM. Management of critically ill adults with COVID-19. JAMA [online ahead of print] 26 Mar 2020; DOI: 10.1001/jama.2020.4914. 3. Sanders JM, Monogue ML, Jodlowski TZ, Cutrell JB. Pharmacologic treatments for coronavirus disease 2019 (COVID-19): a review. JAMA [online ahead of print] 13 Apr 2020; DOI: 10.1001/jama. 2020.6019. 4. Leiva-Juárez MM, Kolls JK, Evans SE. Lung epithelial cells: therapeutically inducible effectors of antimicrobial defense. Mucosal Immunol 2018;11:21–34. 5. Bals R, Hiemstra PS. Innate immunity in the lung: how epithelial cells fight against respiratory pathogens. Eur Respir J 2004;23:327–333. 6. Bartlett JA, Fischer AJ, McCray PBJ Jr. Innate immune functions of the airway epithelium. Contrib Microbiol 2008;15:147–163. 7. Evans SE, Scott BL, Clement CG, Larson DT, Kontoyiannis D, Lewis RE, et al. Stimulated innate resistance of lung epithelium protects mice broadly against bacteria and fungi. Am J Respir Cell Mol Biol 2010;42: 40–50. 8. Kirkpatrick CT, Wang Y, Leiva Juarez MM, Shivshankar P, Pantaleón Garcı́a J, Plumer AK, et al. Inducible lung epithelial resistance requires multisource reactive oxygen species generation to protect against viral infections. MBio 2018;9:e00696-18.[Published erratum appears in MBio 10:e00496-19.] 9. Duggan JM, You D, Cleaver JO, Larson DT, Garza RJ, Guzmán Pruneda FA, et al. Synergistic interactions of TLR2/6 and TLR9 induce a high level of resistance to lung infection in mice. J Immunol 2011;186: 5916–5926. 10. Evans SE, Xu Y, Tuvim MJ, Dickey BF. Inducible innate resistance of lung epithelium to infection. Annu Rev Physiol 2010;72: 413–435. 11. Fehr AR, Stanley P. Coronaviruses: an overview of their replication and pathogenesis. Methods Mol Biol 2015;1282:1–23. 12. Corman VM, Muth D, Niemeyer D, Drosten C. Hosts and sources of endemic human coronaviruses. Adv Virus Res 2018;100: 163–188. 13. Walls AC, Park Y-J, Tortorici MA, Wall A, McGuire AT, Veesler D, et al. Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein. Cell 2020;181:281–292, e6. 14. Tseng CT, Huang C, Newman P, Wang N, Narayanan K, Watts DM, et al. Severe acute respiratory syndrome coronavirus infection of mice transgenic for the human Angiotensin-converting enzyme 2 virus receptor. J Virol 2007;81:1162–1173. 15. Goldblatt DL, Flores JR, Valverde Ha G, Jaramillo AM, Tkachman S, Kirkpatrick CT, et al. Inducible epithelial resistance against acute Sendai virus infection prevents chronic asthma-like lung disease in mice. Br J Pharmacol 2020;177:2256–2273.

Tanner L. Hedrick

Brian P. Murray

Robert S. Hagan

Jason R. Mock

COVID-19: Clean up on IL-6

Section:ChooseTop of pageAbstract <<CONTENTSI. STATEMENT OF THE PROBL...II. WHAT IS BEING MODELED...III. METHODOLOGYIV. RESULTS: FEATURES AND...V. PRACTICAL ASPECTS OF M...VI. CRITICAL ASSESSMENT O...VII. LIMITATIONSVIII. SUMMARY AND CONCLUS...ReferencesCITING ARTICLES

Gustavo Matute-Bello

Gregory Downey

Bethany B. Moore

Steve D. Groshong

Michael A. Matthay

Arthur S. Slutsky

Wolfgang M. Kuebler

An Official American Thoracic Society Workshop Report: Features and Measurements of Experimental Acute Lung Injury in Animals

美国胸科学会官方研讨会报告：动物实验性急性肺损伤的特征与测量

Progressive pulmonary fibrosis results from a dysfunctional tissue repair response and is characterized by fibroblast proliferation, activation, and invasion and extracellular matrix accumulation. Lung fibroblast heterogeneity is well recognized. With single-cell RNA sequencing, fibroblast subtypes have been reported by recent studies. However, the roles of fibroblast subtypes in effector functions in lung fibrosis are not well understood. In this study, we incorporated the recently published single-cell RNA-sequencing datasets on murine lung samples of fibrosis models and human lung samples of fibrotic diseases and analyzed fibroblast gene signatures. We identified and confirmed the novel fibroblast subtypes we reported recently across all samples of both mouse models and human lung fibrotic diseases, including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease, and coronavirus disease (COVID-19). Furthermore, we identified specific cell surface proteins for each fibroblast subtype through differential gene expression analysis, which enabled us to isolate primary cells representing distinct fibroblast subtypes by flow cytometry sorting. We compared matrix production, including fibronectin, collagen, and hyaluronan, after profibrotic factor stimulation and assessed the invasive capacity of each fibroblast subtype. Our results suggest that in addition to myofibroblasts, lipofibroblasts and Ebf1+ (Ebf transcription factor 1+) fibroblasts are two important fibroblast subtypes that contribute to matrix deposition and also have enhanced invasive, proliferative, and contraction phenotypes. The histological locations of fibroblast subtypes are identified in healthy and fibrotic lungs by these cell surface proteins. This study provides new insights to inform approaches to targeting lung fibroblast subtypes to promote the development of therapeutics for lung fibrosis.

Xue Liu

Kristy Dai

Xuexi Zhang

Guanling Huang

Heather Lynn

Anas Rabata

Jiurong Liang

Paul W. Noble

Dianhua Jiang

Multiple Fibroblast Subtypes Contribute to Matrix Deposition in Pulmonary Fibrosis

多种成纤维细胞亚型参与肺纤维化中的基质沉积

Severe lung injury requiring mechanical ventilation may lead to secondary fibrosis. Senescence, a cell response characterized by cell cycle arrest and a shift towards a proinflammatory/profibrotic phenotype, is one of the involved mechanisms. Here, we explore the contribution of mechanical stretch as trigger of senescence of the respiratory epithelium and its link with fibrosis. Human lung epithelial cells and fibroblasts were exposed

Paula Martín-Vicente

Cecilia López-Martínez

Inés López-Alonso

Sara M Exojo-Ramírez

Israel David Duarte-Herrera

Laura Amado-Rodríguez

Irene Ordoñez

Elias Cuesta-Llavona

Juan Gómez

Natalia Campo

Cecilia M. O'Kane

Daniel F. McAuley

Covadonga Huidobro

Guillermo M. Albaiceta

Mechanical Stretch Induces Senescence of Lung Epithelial Cells and Drives Fibroblast Activation by Paracrine Mechanisms

机械拉伸诱导肺上皮细胞衰老并通过旁分泌机制驱动成纤维细胞激活

Airway epithelial cells (AECs) play an essential role in the immune response during bacterial pneumonia. Secreted and transmembrane 1a (Sectm1a) is specifically expressed in AECs during early

Hiromu Tanaka

Hirofumi Kamata

Makoto Ishii

Takanori Asakura

Ho Namkoong

Kensuke Nakagawara

Atsuho Morita

Tatsuya Kusumoto

Shuhei Azekawa

Masanori Kaji

Genta Nagao

Naoki Fukunaga

Tomoyasu Nishimura

Keisuke Asakura

Naoki Hasegawa

Koichi Fukunaga

Sectm1a Depletion Promotes Neutrophil Recruitment during Pneumococcal Pneumonia

Sectm1a耗竭促进中性粒细胞在肺炎球菌性肺炎中的招募

Asthma is a heterogeneous disease with variable presentation and characteristics. There is a critical need to identify underlying molecular endotypes of asthma. We performed the largest transcriptomic analysis of 808 bronchial epithelial cell (BEC) samples across 11 independent cohorts, including 3 cohorts from the Severe Asthma Research Program (SARP). Using 7 datasets (218 asthma patients, 148 healthy controls) as discovery cohorts, we identified 505 differentially expressed genes (DEGs), which we validated in the remaining four datasets. Unsupervised clustering using the 505 DEGs identified four reproducible clusters of patients with asthma across all datasets corresponding to healthy controls, mild/moderate asthma, and severe asthma with significant differences in several clinical markers of severity, including pulmonary function, T2 inflammation, FeNO, and max bronchodilator reversibility. Importantly, we found the same clusters in pediatric patients using nasal lavage fluid cells, demonstrating the gene signature and clusters are not confounded by age and conserved in both lower and upper airways. The four asthma clusters may represent a unifying framework for understanding the molecular heterogeneity of asthma. Further study could potentially enable a precision medicine approach of matching therapies with asthma patients most likely to benefit.

Ian Lee

Ananthakrishnan Ganesan

Laurynas Kalesinskas

Hong Zheng

Haejun C. Ahn

Stephanie Christenson

Serpil C Erzurum

Joe Zein

Eugene R Bleecker

Deborah A. Meyers

Mario Castro

John V Fahy

Elliot Israel

Nizar N Jarjour

Wendy Moore

Sally E. Wenzel

David T Mauger

Bruce D. Levy

Prescott G. Woodruff

Victor E. Ortega

Purvesh Khatri

Multicohort Analysis of Bronchial Epithelial Cell Expression in Healthy Subjects and Patients with Asthma Reveals Four Clinically Distinct Clusters

多队列分析揭示健康受试者及哮喘患者气道上皮细胞表达的四个临床特异性簇

Acute respiratory distress syndrome (ARDS) results in decreased quality of life, including increased risk of pulmonary hypertension (PH). In animal models, ARDS can be induced by lipopolysaccharide (LPS), which can disrupt the pulmonary endothelium and epithelium and induce inflammation. We tested whether

Emma Lamanna

Zoe F. Kropf

Raymond Luong

Matthew Narayan

Elizabeth A. Richards

Bailey Cardwell

Simon G Royce

Claudia A Nold-Petry

Jane E. Bourke

LPS Increases Artery but Not Airway Contraction in Precision Cut Lung Slices from a Mouse Model of ARDS

LPS在ARDS小鼠模型精确切割肺切片中增加动脉收缩但不增加气道收缩

Congenital diaphragmatic hernia (CDH) is characterized by incomplete closure of the diaphragm. While the ensuing compression to the fetal lung causes lung hypoplasia, specific cellular phenotypes and developmental signaling defects in the alveolar epithelium in CDH are not fully understood. Employing lung samples from human CDH, a surgical lamb model and a nitrogen rat model, we investigate whether lung compression impairs alveolar epithelial differentiation and Yes-associated protein (YAP)-mediated mechanosensing. We showed that CDH in humans and lambs caused defective alveolar epithelial differentiation manifested by more abundant ATII cells, fewer ATI cells, and the emergence of cells expressing both ATI and ATII markers. Associated with the alveolar epithelial defects, we found a decrease in the level and nuclear localization of YAP. Reduced nuclear YAP and abnormal distal lung development were evident as early as 21 weeks in gestation in human CDH. In addition, rat fetuses with CDH also showed diminished nuclear YAP and mor abundant ATII cells. In contrast, the littermates without the hernia had no such alveolar phenotypes. Furthermore, fetal tracheal occlusion (TO) in the surgical lamb model of CDH fully normalized nuclear YAP and rescued alveolar epithelial defects in a gestational age-dependent manner. Taken together, our findings across species indicate that lung compression in CDH is sufficient to disrupt alveolar epithelial differentiation and impair YAP signaling. TO can restore nuclear YAP and rescue the alveolar defects in CDH, depending on the timing and the duration of this prenatal surgical intervention. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Ophelia Aubert

Yuichiro Miyake

Gaurang M. Amonkar

Olivia M Dinwoodie

Brian M. Varisco

Mario Marotta

Caiqi Zhao

Richard Wagner

Ya-Wen Chen

Alessandra Moscatello

Caterina Tiozzo

Xaralabos Varelas

Paul H Lerou

Jose L. Peiro

Richard Keijzer

Xingbin Ai

Fetal Tracheal Occlusion Corelates with Normalized YAP Expression and Alveolar Epithelial Differentiation in CDH

Abbreviation	Am J Respir Cell Mol Biol
Journal Impact	6.02
Quartiles(Global)	RESPIRATORY SYSTEM(Q1)

ISSN	1044-1549, 1535-4989
h-index	178

Publication Information	Publisher: American Thoracic Society，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1989，Proportion of original research papers: 94.90%，Self Citation Rate:5.10%， Gold OA Rate: 12.42%
Average review cycle	网友分享经验：一般,3-8周
Average recruitment ratio	网友分享经验：较难

American Journal of Respiratory Cell and Molecular Biology

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