Hydrogen sulfide is emerging as an important mediator of many aspects of inflammation, and perhaps most importantly as a factor promoting the resolution of inflammation and repair of injury. Enteric bacteria can be a significant source of H2S, which could affect mucosal integrity; indeed, luminal H2S can serve as an alternative to oxygen as a metabolic substrate for mitochondrial respiration in epithelial cells. Enterocytes and colonocytes thereby represent a ‘‘metabolic barrier’’ to the diffusion of bacteria-derived H2S into the subepithelial space. A compromise of this barrier could result in modulation of mucosal function and integrity by bacterial H2S.
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