Browsing by Subject "H2S"

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    Hydrogen sulfide therapy improves intestinal recovery through endothelial nitric oxide dependent mechanisms
    (2017) Jensen, Amanda; Markel, Troy
    H2S is a gaseous mediator that acts as an anti-inflammatory agent contributing to gastrointestinal mucosal defense. It promotes vascular dilation, mucosal repair, and resolution of inflammation following intestinal ischemia and may be exploited as a novel therapeutic agent. It is unclear if H2S works through nitric oxide-dependent pathways in the intestine. We appreciated that H2S was able to improve post-ischemic recovery of mesenteric perfusion, mucosal integrity, and inflammation. The beneficial effects of H2S appear to be mediated through endothelial nitric oxide-dependent pathways.
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    Shifts in the Fecal Microbiota Associated with Adenomatous Polyps
    (American Association for Cancer Research, 2017-01) Hale, Vanessa L.; Chen, Jun; Johnson, Stephen; Harrington, Sean C.; Yab, Tracy C.; Smyrk, Thomas C.; Nelson, Heidi; Boardman, Lisa A.; Druliner, Brooke R.; Levin, Theodore R.; Rex, Douglas K.; Ahnen, Dennis J.; Lance, Peter; Ahlquist, David A.; Chia, Nicholas; Medicine, School of Medicine
    BACKGROUND: Adenomatous polyps are the most common precursor to colorectal cancer, the second leading cause of cancer-related death in the United States. We sought to learn more about early events of carcinogenesis by investigating shifts in the gut microbiota of patients with adenomas. METHODS: We analyzed 16S rRNA gene sequences from the fecal microbiota of patients with adenomas (n = 233) and without (n = 547). RESULTS: Multiple taxa were significantly more abundant in patients with adenomas, including Bilophila, Desulfovibrio, proinflammatory bacteria in the genus Mogibacterium, and multiple Bacteroidetes species. Patients without adenomas had greater abundances of Veillonella, Firmicutes (Order Clostridia), and Actinobacteria (family Bifidobacteriales). Our findings were consistent with previously reported shifts in the gut microbiota of colorectal cancer patients. Importantly, the altered adenoma profile is predicted to increase primary and secondary bile acid production, as well as starch, sucrose, lipid, and phenylpropanoid metabolism. CONCLUSIONS: These data hint that increased sugar, protein, and lipid metabolism along with increased bile acid production could promote a colonic environment that supports the growth of bile-tolerant microbes such as Bilophilia and Desulfovibrio In turn, these microbes may produce genotoxic or inflammatory metabolites such as H2S and secondary bile acids, which could play a role in catalyzing adenoma development and eventually colorectal cancer. IMPACT: This study suggests a plausible biological mechanism to explain the links between shifts in the microbiota and colorectal cancer. This represents a first step toward resolving the complex interactions that shape the adenoma-carcinoma sequence of colorectal cancer and may facilitate personalized therapeutics focused on the microbiota.