The Key Lab of Animal Disease and Public Health, Henan University of Science and Technology, Luoyang, 471023, Henan, China; Luoyang Key Laboratory of Live Carrier Biomaterial and Animal Disease Prevention and Control, Luoyang, 471023, Henan, China.
The Key Lab of Animal Disease and Public Health, Henan University of Science and Technology, Luoyang, 471023, Henan, China; Luoyang Key Laboratory of Live Carrier Biomaterial and Animal Disease Prevention and Control, Luoyang, 471023, Henan, China.
Microb Pathog. 2018 Apr;117:270-275. doi: 10.1016/j.micpath.2018.02.030. Epub 2018 Feb 17.
Salmonella enteritidis is a common food-borne pathogen associated with consumption of contaminated poultry meat and eggs, which frequently causes gastroenteritis in humans. Salmonella secreted effector K1 (SseK1), as a translocated and secreted protein has been identified to be essential for the virulence of Salmonella typhimurium in host cells. However, the role of the sseK1 gene in the pathogenicity of S. enteritidis remain unclear. In this study, a sseK1 deletion mutant of S. enteritidis was constructed and its biological characteristics were examined. It was found that the sseK1 deletion mutant did not affect the growth, adherence and invasion of Salmonella enteritidis when compared to the wild-type S. enteritidis. However, the mutant showed decreased formation of biofilm and significantly reduced intracellular survival of bacteria in activated mouse peritoneal macrophages, as well as showed reduced pathogenicity to a murine model by increasing the lethal dose 50% (LD) value and decreasing the proliferation ratio of bacteria in vivo. Taken together, this study determined an important role for SseK1 in the pathogenicity of S. enteritidis in vitro and in vivo.
肠炎沙门氏菌是一种常见的食源性病原体,与食用受污染的禽肉和蛋类有关,常引起人类肠胃炎。沙门氏菌分泌效应子 K1(SseK1)作为一种易位和分泌蛋白,已被确定对鼠伤寒沙门氏菌在宿主细胞中的毒力至关重要。然而,sseK1 基因在肠炎沙门氏菌致病性中的作用尚不清楚。在本研究中,构建了肠炎沙门氏菌 sseK1 缺失突变体,并检测了其生物学特性。结果发现,与野生型肠炎沙门氏菌相比,sseK1 缺失突变体对肠炎沙门氏菌的生长、黏附和侵袭没有影响。然而,该突变体在活化的小鼠腹腔巨噬细胞中形成生物膜的能力下降,细菌的胞内存活能力显著降低,并且通过增加半数致死剂量 (LD) 值和降低体内细菌增殖率,使肠炎沙门氏菌对小鼠模型的致病性降低。综上所述,本研究确定了 SseK1 在肠炎沙门氏菌体外和体内致病性中的重要作用。