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The respiratory tract microbiome and lung inflammation: a two-way street.
Open accessAbstract
The lungs are not sterile or free from bacteria; rather, they harbor a distinct microbiome whose composition is driven by different ecological rules than for the gastrointestinal tract. During disease, there is often a shift in community composition towards Gammaproteobacteria, the bacterial class that contains many common lung-associated gram-negative "pathogens." Numerous byproducts of host inflammation are growth factors for these bacteria. The extracellular nutrient supply for bacteria in the lungs, which is severely limited during health, markedly increases due to the presence of mucus and vascular permeability. While Gammaproteobacteria benefit from airway inflammation, they also encode molecular components that promote inflammation, potentially creating a cyclical inflammatory mechanism. In contrast, Prevotella species that are routinely acquired via microaspiration from the oral cavity may participate in immunologic homeostasis of the airways.vAreas of future research include determining for specific lung diseases (1) whether an altered lung microbiome initiates disease pathogenesis, promotes chronic inflammation, or is merely a marker of injury and inflammation, (2) whether the lung microbiome can be manipulated therapeutically to change disease progression, (3) what molecules (metabolites) generated during an inflammatory response promote cross-kingdom signaling, and (4) how the lung "ecosystem" collapses during pneumonia, to be dominated by a single pathogen.
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“Prevotella from microaspiration, can also participate in the immune homeostasis of the respiratory tract (Huffnagle et al., 2017).”
From Oral Microbiome and SARS-CoV-2: Beware of Lung Co-infection (2020) · cites this paper as Huffnagle et al., 2017
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Metadata
- Authors
- Huffnagle, G. B., Dickson, R. P., & Lukacs, N. W.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Huffnagle, G.B.
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2017-03
- Volume
- 10
- Issue
- 2
- Pages
- 299-306
- ISSN
- 1933-0219 (ISSN-L)
- PMC
- PMC5765541
- OpenAlex
- W2561758149
- Cited by
- 535
- References
- 75
- Citations by year
- 2026: 42 · 2025: 60 · 2024: 73 · 2023: 60 · 2022: 84 · 2021: 94 · 2020: 61 · 2019: 21 · 2018: 26 · 2017: 12
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Michigan (UL1TR000433)
- National Institutes of Health (UL1TR000433)
- National Heart, Lung, and Blood Institute (U01HL098961, ROI-HL114447, R01HL114858, K23HL130641, R01HL114447, T32HL007749)
- National Institute of Allergy and Infectious Diseases (AI-036302, R01AI036302)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
- Keywords
- airway microbiome, lung inflammation, Gammaproteobacteria, Gram-negative pathogens, Prevotella, mucus, vascular permeability, host-microbe interactions, chronic inflammation, pneumonia, microaspiration
- MeSH terms
- Animals, Capillary Permeability, Homeostasis, Humans, Lung Diseases, Pneumonia, Respiratory System, Prevotella, Gammaproteobacteria, Host-Pathogen Interactions, Microbiota, Dysbiosis
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