Hydrogen sulfide: an agent of stability at the microbiome-mucosa interface

A diverse range of effects of the intestinal microbiota on mucosal defense and injury has become increasingly clear over the past decade. Hydrogen sulfide (H S) has emerged as an important mediator of many physiological functions, including gastrointestinal mucosal defense and repair. Hydrogen sulfi...

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Veröffentlicht in:American journal of physiology: Gastrointestinal and liver physiology 2018-02, Vol.314 (2), p.G143-G149
Hauptverfasser: Wallace, John L, Motta, Jean-Paul, Buret, Andre G
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Sprache:eng
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Zusammenfassung:A diverse range of effects of the intestinal microbiota on mucosal defense and injury has become increasingly clear over the past decade. Hydrogen sulfide (H S) has emerged as an important mediator of many physiological functions, including gastrointestinal mucosal defense and repair. Hydrogen sulfide is produced by gastrointestinal tract tissues and by bacteria residing within the gut and can influence the function of a wide range of cells. The microbiota also appears to be an important target of hydrogen sulfide. H S donors can modify the gut microbiota, and the gastrointestinal epithelium is a major site of oxidation of microbial-derived H S. When administered together with nonsteroidal anti-inflammatory drugs, H S can prevent some of the dysbiosis those drugs induce, possibly contributing to the observed prevention of gastrointestinal damage. Exogenous H S can also markedly reduce the severity of experimental colitis and plays important roles in modulating epithelial cell-mucus-bacterial interactions in the intestine, contributing to its ability to promote resolution of inflammation and repair of tissue injury. In this paper we review recent studies examining the roles of H S in mucosal defense, the possibility that H S can damage the gastrointestinal epithelium, and effects of H S on the gut microbiota and on mucus and biofilm interactions in the context of intestinal inflammation.
ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.00249.2017