title: A tale of two sites: how inflammation can reshape the microbiomes of the gut and lungs.
abstract: Inflammation can directly and indirectly modulate the bacterial composition of the microbiome. Although studies of inflammation primarily focus on its function to negatively select against potential pathogens, some bacterial species have the ability to exploit inflammatory byproducts for their benefit. Inflammatory cells release reactive nitrogen species as antimicrobial effectors against infection, but some facultative anaerobes can also utilize the increase in extracellular nitrate in their environment for anaerobic respiration and growth. This phenomenon has been studied in the gastrointestinal tract, where blooms of facultative anaerobic Gammaproteobacteria, primarily Escherichia coli, often occur during colonic inflammation. In cystic fibrosis, Pseudomonas aeruginosa, another Gammaproteobacteria facultative anaerobe, can reduce nitrogen for anaerobic respiration and it blooms in the airways of the chronically inflamed cystic fibrosis lung. This review focuses on the evidence that inflammation can provide terminal electron acceptors for anaerobic respiration and can support blooms of facultative anaerobes, such as E. coli and P. aeruginosa in distinct, but similar, environments of the inflamed gastrointestinal and respiratory tracts.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA.
authors.forename: Brittan S
authors.initials: BS
authors.lastname: Scales
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA.
authors.forename: Robert P
authors.initials: RP
authors.lastname: Dickson
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA ghuff@umich.edu.
authors.forename: Gary B
authors.initials: GB
authors.lastname: Huffnagle
mesh_terms: D000693:Anaerobiosis; D003092:Colitis / Q000276:immunology / Q000382:microbiology; D003550:Cystic Fibrosis / Q000276:immunology / Q000382:microbiology; D004927:Escherichia coli Infections / Q000276:immunology; D025461:Feedback, Physiological; D020563:Gammaproteobacteria / Q000502:physiology; D000069196:Gastrointestinal Microbiome; D041981:Gastrointestinal Tract / Q000276:immunology / Q000382:microbiology*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D008168:Lung / Q000276:immunology / Q000382:microbiology*; D064307:Microbiota / Q000276:immunology; D009093:Mucus / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D009584:Nitrogen / Q000378:metabolism; D010084:Oxidation-Reduction; D011552:Pseudomonas Infections / Q000276:immunology
chemical_list: D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D009584:Nitrogen
keywords: E. coli; P. aeruginosa; cystic fibrosis; inflammatory bowel disease; nitrate reduction