title: The respiratory tract microbiome and lung inflammation: a two-way street.
abstract: 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.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.|Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.|Mary H. Weiser Food Allergy Center, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: G B
authors.initials: GB
authors.lastname: Huffnagle
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: R P
authors.initials: RP
authors.lastname: Dickson
authors.affiliation: Mary H. Weiser Food Allergy Center, University of Michigan Medical School, Ann Arbor, MI, USA.|Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: N W
authors.initials: NW
authors.lastname: Lukacs
mesh_terms: D000818:Animals; D002199:Capillary Permeability; D064806:Dysbiosis / Q000276:immunology*; D020563:Gammaproteobacteria / Q000276:immunology*; D006706:Homeostasis; D054884:Host-Pathogen Interactions; D006801:Humans; D008171:Lung Diseases / Q000276:immunology / Q000382:microbiology*; D064307:Microbiota; D011014:Pneumonia / Q000276:immunology / Q000382:microbiology*; D018720:Prevotella / Q000276:immunology*; D012137:Respiratory System / Q000276:immunology / Q000382:microbiology*