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首页> 外文期刊>Infection and immunity >The Periplasmic Nitrate Reductase NapABC Supports Luminal Growth of Salmonella enterica Serovar Typhimurium during Colitis
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The Periplasmic Nitrate Reductase NapABC Supports Luminal Growth of Salmonella enterica Serovar Typhimurium during Colitis

机译：周质硝酸还原酶NapABC支持结肠炎期间肠炎沙门氏菌血清型鼠伤寒的发光生长。

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The food-borne pathogen Salmonella enterica serovar Typhimurium benefits from acute inflammation in part by using host-derived nitrate to respire anaerobically and compete successfully 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 found, surprisingly, 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 wild-type S. Typhimurium. 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 the 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 that S. Typhimurium uses the periplasmic nitrate reductase to support its growth on the low nitrate concentrations encountered in the gut, a strategy that may be shared with other enteric pathogens.
机译：食源性病原体小肠鼠伤寒沙门氏菌可从急性炎症中受益，部分原因是使用宿主衍生的硝酸盐厌氧呼吸并在肠腔内生长期间与共生微生物成功竞争。鼠伤寒沙门氏菌基因组包含三种硝酸还原酶，分别由narGHI，narZYV和napABC基因编码。对大肠杆菌中存在的同源基因的研究表明，由narGHI基因编码的硝酸还原酶A是促进厌氧环境中硝酸盐作为电子受体生长的主要酶。使用小鼠结肠炎模型，我们令人惊讶地发现，在高浓度硝酸盐（narL突变体）存在下，硝酸盐还原酶A（narG突变体）或调节剂诱导其转录缺陷的鼠伤寒沙门氏菌菌株表现出与其生长相当的生长。型鼠伤寒沙门氏菌。相反，缺乏功能性周质硝酸还原酶（napA突变体）的菌株在结肠腔中表现出明显的生长缺陷。在大肠杆菌中，在低硝酸盐浓度下，厌氧生长条件下，napABC基因的转录最大。 narP的失活编码响应低硝酸盐浓度而激活napABC转录的应答调节剂，可显着降低鼠伤寒沙门氏菌在肠腔中的生长。盲肠硝酸盐的测量表明，鼠盲肠是硝酸盐受限的环境。总体而言，我们的结果表明，鼠伤寒沙门氏菌利用周质硝酸还原酶来支持肠道中遇到的低硝酸盐浓度下的生长，这种策略可能会与其他肠道病原体共享。

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