The food-borne pathogen Salmonella enterica serovar Typhimurium benefits from acute inflammation in part by using host-derived nitrate to anaerobically respire and successfully compete with the commensal microbes during growth in the intestinal lumen. The S. Typhimurium genome contains three nitrate reductases encoded by the narGHI, narZYV and napABC genes. Work on homologous genes present in Escherichia coli suggests that nitrate reductase A encoded by the narGHI genes is the main enzyme promoting growth on nitrate as an electron acceptor in anaerobic environments. Using a mouse colitis model, we surprisingly found that S. Typhimurium strains with defects in either nitrate reductase A (narG mutant) or the regulator inducing its transcription in the presence of high concentrations of nitrate (narL mutant) exhibited growth comparable to that of the S. Typhimurium wild type. In contrast, a strain lacking a functional periplasmic nitrate reductase (napA mutant) exhibited a marked growth defect in the lumen of the colon. In E. coli, the napABC genes are transcribed maximally under anaerobic growth conditions in the presence of low nitrate concentrations. Inactivation of narP, encoding a response regulator that activates napABC transcription in response to low nitrate concentrations, significantly reduced growth of S. Typhimurium in the gut lumen. Cecal nitrate measurements suggested that the murine cecum is a nitrate-limited environment. Collectively, our results suggest S. Typhimurium uses the periplasmic nitrate reductase to support its growth on low nitrate concentrations encountered in the gut, a strategy that may be shared with other enteric pathogens.
This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 27 June 2015.
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