A tale of two sites: how inflammation can reshape the microbiomes of the gut and lungs. Issue 5 (30th June 2016)

• Record Type: Journal Article
• Authors: Scales, Brittan S; Dickson, Robert P; Huffnagle, Gary B
• Is Part Of: Journal of leukocyte biology. Volume 100:Issue 5(2016)
• Page Start: 943
• Page End: 950
• Publication Date: 2016-06-30
• Subjects: nitrate reduction -- E. coli -- P. aeruginosa -- cystic fibrosis -- inflammatory bowel disease; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.3MR0316-106R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : Review on how mucosal inflammation benefits facultative anaerobes, leading to blooms of Gammaproteobacteria in the microbiota of the GI and respiratory tracts. 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.