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细胞内细菌如何存活:促进对宿主固有免疫反应产生抗性的表面修饰。

How intracellular bacteria survive: surface modifications that promote resistance to host innate immune responses.

作者信息

Ernst R K, Guina T, Miller S I

机构信息

Department of Medicine, University of Washington, Seattle 98195, USA.

出版信息

J Infect Dis. 1999 Mar;179 Suppl 2:S326-30. doi: 10.1086/513850.

DOI:10.1086/513850
PMID:10081503
Abstract

Bacterial pathogens regulate the expression of virulence factors in response to environmental signals. In the case of salmonellae, many virulence factors are regulated via PhoP/PhoQ, a two-component signal transduction system that is repressed by magnesium and calcium in vitro. PhoP/PhoQ-activated genes promote intracellular survival within macrophages, whereas PhoP-repressed genes promote entrance into epithelial cells and macrophages by macropinocytosis and stimulate epithelial cell cytokine production. PhoP-activated genes include those that alter the cell envelope through structural alterations of lipopolysaccharide and lipid A, the bioactive component of lipopolysaccharide. PhoP-activated changes in the bacterial envelope likely promote intracellular survival by increasing resistance to host cationic antimicrobial peptides and decreasing host cell cytokine production.

摘要

细菌病原体根据环境信号调节毒力因子的表达。就沙门氏菌而言,许多毒力因子是通过PhoP/PhoQ调节的,PhoP/PhoQ是一种双组分信号转导系统,在体外受镁和钙的抑制。PhoP/PhoQ激活的基因促进巨噬细胞内的存活,而PhoP抑制的基因通过巨吞饮作用促进进入上皮细胞和巨噬细胞,并刺激上皮细胞产生细胞因子。PhoP激活的基因包括那些通过脂多糖和脂质A(脂多糖的生物活性成分)的结构改变来改变细胞包膜的基因。细菌包膜中PhoP激活的变化可能通过增加对宿主阳离子抗菌肽的抗性和减少宿主细胞细胞因子的产生来促进细胞内存活。

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