دورية أكاديمية
Lower Airway Dysbiosis Augments Lung Inflammatory Injury in Mild-to-Moderate Chronic Obstructive Pulmonary Disease.
| العنوان: | Lower Airway Dysbiosis Augments Lung Inflammatory Injury in Mild-to-Moderate Chronic Obstructive Pulmonary Disease. |
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| المؤلفون: | Sulaiman I; Division of Pulmonary and Critical Care Medicine.; Department of Medicine.; Department of Respiratory Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland.; Department of Respiratory Medicine, Beaumont Hospital, Dublin, Ireland., Wu BG; Division of Pulmonary and Critical Care Medicine.; Department of Medicine.; Division of Pulmonary and Critical Care Medicine, Veterans Affairs (VA) New York Harbor Healthcare System, New York, New York., Chung M; Systems Genomics Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland., Isaacs B; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Tsay JJ; Division of Pulmonary and Critical Care Medicine.; Department of Medicine.; Division of Pulmonary and Critical Care Medicine, Veterans Affairs (VA) New York Harbor Healthcare System, New York, New York., Holub M; Division of Pulmonary and Critical Care Medicine.; Department of Medicine.; Division of Pulmonary and Critical Care Medicine, Hartford Health Care, Hartford, Connecticut., Barnett CR; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Kwok B; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Kugler MC; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Natalini JG; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Singh S; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Li Y; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Schluger R; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Carpenito J; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Collazo D; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Perez L; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Kyeremateng Y; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Chang M; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Campbell CD; Department of Respiratory Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland.; Department of Respiratory Medicine, Beaumont Hospital, Dublin, Ireland., Hansbro PM; Centre for Inflammation, Centenary Institute and University of Technology Sydney, School of Life Sciences, Sydney, New South Wales, Australia., Oppenheimer BW; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Berger KI; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Goldring RM; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Koralov SB; Department of Pathology, and., Weiden MD; Division of Pulmonary and Critical Care Medicine.; Department of Medicine., Xiao R; Department of Physiology and Cellular Biophysics, Columbia University School of Medicine, New York, New York; and., D'Armiento J; Department of Physiology and Cellular Biophysics, Columbia University School of Medicine, New York, New York; and., Clemente JC; Department of Genetics and Genomic Sciences and Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York., Ghedin E; Systems Genomics Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland., Segal LN; Division of Pulmonary and Critical Care Medicine.; Department of Medicine.; Laura and Isaac Perlmutter Cancer Center, New York University Grossman School of Medicine, New York University (NYU) Langone Health, New York, New York. |
| المصدر: | American journal of respiratory and critical care medicine [Am J Respir Crit Care Med] 2023 Nov 15; Vol. 208 (10), pp. 1101-1114. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Thoracic Society Country of Publication: United States NLM ID: 9421642 Publication Model: Print Cited Medium: Internet ISSN: 1535-4970 (Electronic) Linking ISSN: 1073449X NLM ISO Abbreviation: Am J Respir Crit Care Med Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2000- : New York, NY : American Thoracic Society Original Publication: New York, NY : American Lung Association, c1994- |
| مواضيع طبية MeSH: | Pulmonary Disease, Chronic Obstructive*/genetics , Lung Injury*/complications, Humans ; Animals ; Mice ; Dysbiosis/complications ; RNA, Ribosomal, 16S ; Inflammation/complications ; Lung/pathology |
| مستخلص: | Rationale: Chronic obstructive pulmonary disease (COPD) is associated with high morbidity, mortality, and healthcare costs. Cigarette smoke is a causative factor; however, not all heavy smokers develop COPD. Microbial colonization and infections are contributing factors to disease progression in advanced stages. Objectives: We investigated whether lower airway dysbiosis occurs in mild-to-moderate COPD and analyzed possible mechanistic contributions to COPD pathogenesis. Methods: We recruited 57 patients with a >10 pack-year smoking history: 26 had physiological evidence of COPD, and 31 had normal lung function (smoker control subjects). Bronchoscopy sampled the upper airways, lower airways, and environmental background. Samples were analyzed by 16S rRNA gene sequencing, whole genome, RNA metatranscriptome, and host RNA transcriptome. A preclinical mouse model was used to evaluate the contributions of cigarette smoke and dysbiosis on lower airway inflammatory injury. Measurements and Main Results: Compared with smoker control subjects, microbiome analyses showed that the lower airways of subjects with COPD were enriched with common oral commensals. The lower airway host transcriptomics demonstrated differences in markers of inflammation and tumorigenesis, such as upregulation of IL-17, IL-6, ERK/MAPK, PI3K, MUC1, and MUC4 in mild-to-moderate COPD. Finally, in a preclinical murine model exposed to cigarette smoke, lower airway dysbiosis with common oral commensals augments the inflammatory injury, revealing transcriptomic signatures similar to those observed in human subjects with COPD. Conclusions: Lower airway dysbiosis in the setting of smoke exposure contributes to inflammatory injury early in COPD. Targeting the lower airway microbiome in combination with smoking cessation may be of potential therapeutic relevance. |
| التعليقات: | Comment in: Am J Respir Crit Care Med. 2023 Nov 15;208(10):1019-1021. doi: 10.1164/rccm.202309-1599ED. (PMID: 37703423) |
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| معلومات مُعتمدة: | UL1 TR001445 United States TR NCATS NIH HHS; P30 CA016087 United States CA NCI NIH HHS; T32 ES007324 United States ES NIEHS NIH HHS; U2C CA271890 United States CA NCI NIH HHS; L30 AI138249 United States AI NIAID NIH HHS; IK2 BX005309 United States BX BLRD VA; K23 AI102970 United States AI NIAID NIH HHS; R37 CA244775 United States CA NCI NIH HHS; KL2 TR001446 United States TR NCATS NIH HHS; R56 HL151700 United States HL NHLBI NIH HHS; KL2TR001446 United States GF NIH HHS; R21 GM147800 United States GM NIGMS NIH HHS; R01 HL125816 United States HL NHLBI NIH HHS |
| فهرسة مساهمة: | Keywords: COPD; lung inflammation; metatranscriptomics; microbiome; transcriptomics |
| المشرفين على المادة: | 0 (RNA, Ribosomal, 16S) |
| تواريخ الأحداث: | Date Created: 20230907 Date Completed: 20231116 Latest Revision: 20240613 |
| رمز التحديث: | 20240613 |
| مُعرف محوري في PubMed: | PMC10867925 |
| DOI: | 10.1164/rccm.202210-1865OC |
| PMID: | 37677136 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1535-4970 |
|---|---|
| DOI: | 10.1164/rccm.202210-1865OC |