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首页> 外文期刊>Infection and immunity >Glucose and Glycolysis Are Required for the Successful Infection of Macrophages and Mice by Salmonella enterica Serovar Typhimurium
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Glucose and Glycolysis Are Required for the Successful Infection of Macrophages and Mice by Salmonella enterica Serovar Typhimurium

机译：沙门氏菌血清型鼠伤寒沙门氏菌成功感染巨噬细胞和小鼠需要葡萄糖和糖酵解

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Salmonella is a widespread zoonotic enteropathogen that causes gastroenteritis and fatal typhoidal disease in mammals. During systemic infection of mice, Salmonella enterica serovar Typhimurium resides and replicates in macrophages within the “Salmonella-containing vacuole” (SCV). It is surprising that the substrates and metabolic pathways necessary for growth of S. Typhimurium within the SCV of macrophages have not been identified yet. To determine whether S. Typhimurium utilized sugars within the SCV, we constructed a series of S. Typhimurium mutants that lacked genes involved in sugar transport and catabolism and tested them for replication in mice and macrophages. These mutants included a mutant with a mutation in the pfkAB-encoded phosphofructokinase, which catalyzes a key committing step in glycolysis. We discovered that a pfkAB mutant is severely attenuated for replication and survival within RAW 264.7 macrophages. We also show that disruption of the phosphoenolpyruvate:carbohydrate phosphotransferase system by deletion of the ptsHI and crr genes reduces S. Typhimurium replication within RAW 264.7 macrophages. We discovered that mutants unable to catabolize glucose due to deletion of ptsHI, crr, and glk or deletion of ptsG, manXYZ, and glk showed reduced replication within RAW 264.7 macrophages. This study proves that S. Typhimurium requires glycolysis for infection of mice and macrophages and that transport of glucose is required for replication within macrophages.
机译：沙门氏菌是一种广泛的人畜共患性肠病原，可引起哺乳动物的肠胃炎和致命性伤寒病。在小鼠全身感染期间，沙门氏菌血清型鼠伤寒沙门氏菌在“含沙门氏菌的液泡”（SCV）内的巨噬细胞中驻留并复制。令人惊讶的是， S 生长所需的底物和代谢途径。巨噬细胞SCV内的鼠伤寒尚未被鉴定。确定是否 S 。鼠伤寒利用SCV中的糖，我们构建了一系列 S 。缺乏与糖转运和分解代谢有关的基因的鼠伤寒突变体，并测试了它们在小鼠和巨噬细胞中的复制。这些突变体包括在 pfkAB 编码的磷酸果糖激酶中具有突变的突变体，其催化糖酵解中的关键步骤。我们发现， pfkAB 突变体在RAW 264.7巨噬细胞内的复制和生存能力大大减弱。我们还表明，通过删除 ptsHI 和 crr 基因来破坏磷酸烯醇式丙酮酸：碳水化合物磷酸转移酶系统会降低 S 。 RAW 264.7巨噬细胞内的鼠伤寒复制。我们发现突变体由于 ptsHI ， crr 和 glk 的缺失或 ptsG 的缺失而无法代谢葡萄糖。 ， manXYZ 和 glk 显示在RAW 264.7巨噬细胞内复制减少。这项研究证明了 S 。鼠伤寒需要糖酵解来感染小鼠和巨噬细胞，而在巨噬细胞内复制需要转运葡萄糖。

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