Bacterial stimulation of endogenous hydrogen sulfide synthesis: a novel mechanism for resolution and repair in the colon

Hydrogen sulfide (H2S) is an important signaling molecule throughout the gastrointestinal (GI) tract. Colonic H2S synthesis is markedly increased during experimental colitis in rats, and contributes to the resolution of inflammation and healing of ulcers. The triggers responsible for this up‐regulation of colonic H2S synthesis are unclear. Therefore, we tested whether bacterial signals at the epithelial surface may be important stimuli for upregulation of endogenous H2S synthesis, helping drive resolution and mucosal repair. Germ‐free NIH Swiss mice (6 weeks of age; n≥4) were orally gavaged with feces (200 μL; 5% wt/ vol) from mice raised in specific pathogen free (SPF) conditions. Inoculated mice were housed in SPF conditions and euthanized at day 2 or 7 post‐inoculation. Colonic tissue from germ‐free control mice produced very low amounts of H2S. Within 2 days of inoculation with SPF flora, a significant increase in colonic H2S synthesis was observed (>;2‐fold; p<0.05), which further increased to 5‐fold (p<0.01) by 7 days post‐inoculation. We previously found that bacterial‐derived H2S does not contribute to what is measured as colonic H2S synthesis. These results support the hypothesis that bacterial factors can up‐regulate colonic H2S, which could be an important signaling mechanism for driving the repair of mucosal injury. Supported by the Crohn's and Colitis Foundation of Canada (CCFC).

Bacterial stimulation of endogenous hydrogen sulfide synthesis: a novel mechanism for resolution and repair in the colon Conferences