Abstract
Dysbiotic intestinal microbiomes dominated by facultative anaerobes are strongly associated with inflammatory bowel disease (IBD). More recently, data from Baumler and colleagues support a model where mitochondrial dysfunction causes disease-associated dysbiosis by increasing oxygen (O2) availability to the microbiome. We posit that the restoration of epithelial mitochondrial respiration contributes to the restoration of a healthy microbiome dominated by facultative anaerobes such as Firmicutes [that produce short chain fatty acids (SCFA)]. Here, we tested a novel compound (AuPhos) that increases an O2 consumption in intestinal epithelial cells (IECs) thereby reducing O2 availability to the microbiome and promotes a healthy anaerobic environment (and blooms of firmicutes).
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