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Airway Microbiome Dynamics in Exacerbations of Chronic Obstructive Pulmonary Disease
Open accessAbstract
Specific bacterial species are implicated in the pathogenesis of exacerbations of chronic obstructive pulmonary disease (COPD). However, recent studies of clinically stable COPD patients have demonstrated a greater diversity of airway microbiota, whose role in acute exacerbations is unclear. In this study, temporal changes in the airway microbiome before, at the onset of, and after an acute exacerbation were examined in 60 sputum samples collected from subjects enrolled in a longitudinal study of bacterial infection in COPD. Microbiome composition and predicted functions were examined using 16S rRNA-based culture-independent profiling methods. Shifts in the abundance (≥ 2-fold, P < 0.05) of many taxa at exacerbation and after treatment were observed. Microbiota members that were increased at exacerbation were primarily of the Proteobacteria phylum, including nontypical COPD pathogens. Changes in the bacterial composition after treatment for an exacerbation differed significantly among the therapy regimens clinically prescribed (antibiotics only, oral corticosteroids only, or both). Treatment with antibiotics alone primarily decreased the abundance of Proteobacteria, with the prolonged suppression of some microbiota members being observed. In contrast, treatment with corticosteroids alone led to enrichment for Proteobacteria and members of other phyla. Predicted metagenomes of particular microbiota members involved in these compositional shifts indicated exacerbation-associated loss of functions involved in the synthesis of antimicrobial and anti-inflammatory products, alongside enrichment in functions related to pathogen-elicited inflammation. These trends reversed upon clinical recovery. Further larger studies will be necessary to determine whether specific compositional or functional changes detected in the airway microbiome could be useful indicators of exacerbation development or outcome.
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“With remarkable consistency, all studies report no increase in bacterial burden and no decrease in community diversity during exacerbations.”
From The microbiome and critical illness (2016) · cites this paper as [132]
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Metadata
- Authors
- Huang, Y. J., Sethi, S., Murphy, T., Nariya, S., Boushey, H. A., & Lynch, S. V.
- Affiliations
- University of California, San Francisco (US)
- Buffalo VA Medical Center (US)
- University at Buffalo, State University of New York (US)
- Venue
- Journal of Clinical Microbiology
- Publisher
- American Society for Microbiology
- Published
- 2014-08
- Volume
- 52
- Issue
- 8
- Pages
- 2813-2823
- ISSN
- 0095-1137 (ISSN-L)
- 1098-660X
- PMC
- PMC4136157
- OpenAlex
- W2135623379
- Cited by
- 323
- References
- 48
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 25 · 2023: 25 · 2022: 30 · 2021: 33 · 2020: 35 · 2019: 28 · 2018: 24 · 2017: 38 · 2016: 27 · 2015: 29 · 2014: 6
- FWCI
- 26.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Microbiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (K23HL105572, HL105572)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Keywords
- chronic obstructive pulmonary disease, COPD exacerbations, airway microbiome, sputum microbiota, Proteobacteria, antibiotic therapy, oral corticosteroids, inflammation
- MeSH terms
- Aged, Aged, 80 and over, DNA, Bacterial, DNA, Ribosomal, Humans, Longitudinal Studies, Male, Middle Aged, Phylogeny, Respiratory System, RNA, Ribosomal, 16S, Sputum, Cluster Analysis, Sequence Analysis, DNA, Proteobacteria, Pulmonary Disease, Chronic Obstructive, Microbiota
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