Caroline C. Gillis

TL;DR: It is shown that a dysbiotic expansion of Enterobacteriaceae during gut inflammation could be prevented by tungstate treatment, which selectively inhibited molybdenum-cofactor-dependent microbial respiratory pathways that are operational only during episodes of inflammation.

TL;DR: Bacterial formate oxidation and oxygen respiration are identified as metabolic signatures for inflammation-associated dysbiosis, which is characterized by a reduced abundance of obligate anaerobic bacteria and an expansion of facultative Proteobacteria such as commensal E. coli.

TL;DR: It is concluded that alterations of the gut microbiota, specifically a depletion of Clostridia, reprogram host metabolism to perform lactate fermentation, thus supporting Salmonella infection.

TL;DR: It is shown that inflammation-derived electron acceptors induce a complete, oxidative TCA cycle in S. Typhimurium, allowing the bacteria to compete with the microbiota for colonization and to utilize a variety of carbon sources, including microbiota-derived succinate.

TL;DR: It is concluded that epithelial-derived reactive oxygen species are degraded in the gut lumen, which gives rise to molecular oxygen that supports the aerobic respiration of E. coli through AppBCX-mediated respiration in a catalase-dependent manner.