Ding Ke, Zhang Chunjie, Li Jing, Chen Songbiao, Liao Chengshui, Cheng Xiangchao, Yu Chuang, Yu Zuhua, Jia Yanyan
The Key Lab of Animal Disease and Public Healthy, Henan University of Science and Technology, Luoyang, China.
Luoyang Key Laboratory of Live Carrier Biomaterial and Animal Disease Prevention and Control, Luoyang, China.
Curr Microbiol. 2019 Jan;76(1):1-6. doi: 10.1007/s00284-018-1574-1. Epub 2018 Oct 12.
We studied the role of glycolysis in the mechanism of cAMP receptor protein-induced macrophage cell death of Salmonella enterica serovar Typhimurium (S. Typhimurium). Cell apoptosis, caspase-3, -8, -9 enzyme activity, and pyruvic acid, lactic acid, ATP, and hexokinase (HK) contents were determined after infection of macrophages with S. Typhimurium SL1344 wild-type and a cAMP receptor protein mutant strain. While cell apoptosis, caspase-3, -8, -9 enzyme activity, lactic acid, hexokinase, and ATP levels significantly changed by infection with crp mutants compared to the wild-type strain (P < 0.05). Our data suggest that the cAMP receptor protein of S. Typhimurium can modulate macrophage death by effecting glycolysis levels. This finding may help to elucidate the mechanisms of S. Typhimurium pathogenesis.
我们研究了糖酵解在鼠伤寒沙门氏菌(Salmonella enterica serovar Typhimurium,简称鼠伤寒沙门菌)环磷酸腺苷(cAMP)受体蛋白诱导巨噬细胞死亡机制中的作用。在用鼠伤寒沙门菌SL1344野生型菌株和cAMP受体蛋白突变株感染巨噬细胞后,测定细胞凋亡、半胱天冬酶-3、-8、-9的酶活性以及丙酮酸、乳酸、三磷酸腺苷(ATP)和己糖激酶(HK)的含量。与野生型菌株相比,感染crp突变株后细胞凋亡、半胱天冬酶-3、-8、-9的酶活性、乳酸、己糖激酶和ATP水平均发生了显著变化(P < 0.05)。我们的数据表明,鼠伤寒沙门菌的cAMP受体蛋白可通过影响糖酵解水平来调节巨噬细胞死亡。这一发现可能有助于阐明鼠伤寒沙门菌的致病机制。