Shigella Infection of Intestinal Epithelium and Circumvention of the Host Innate Defense System

被引:24
作者
Ashida, Hiroshi
Ogawa, Michinaga
Mimuro, Hitomi
Sasakawa, Chihiro [1 ,2 ]
机构
[1] Univ Tokyo, Inst Med Sci, Int Res Ctr Infect Dis, Dept Microbiol & Immunol,Minato Ku, Tokyo 1088639, Japan
[2] Univ Tokyo, Inst Med Sci, Int Res Ctr Infect Dis, Dept Infect Dis Control,Minato Ku, Tokyo 1088639, Japan
来源
MOLECULAR MECHANISMS OF BACTERIAL INFECTION VIA THE GUT | 2009年 / 337卷
基金
日本科学技术振兴机构;
关键词
ACTIN-BASED MOTILITY; NF-KAPPA-B; III SECRETION APPARATUS; CELL-CYCLE PROGRESSION; E3 UBIQUITIN LIGASES; ESCHERICHIA-COLI; GENE-EXPRESSION; BACTERIAL INVASION; VIRULENCE PLASMID; IMMUNE-RESPONSES;
D O I
10.1007/978-3-642-01846-6_8
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Shigella, Gram-negative bacteria closely related to Escherichia coli, are highly adapted human pathogens that cause bacillary dysentery. Although Shigella have neither adherence factors nor flagella required for attaching or accessing the intestinal epithelium, Shigella are capable of colonizing the intestinal epithelium by exploiting epithelial-cell functions and circumventing the host innate immune response. During Shigella infection, they deliver many numbers of effectors through the type III secretion system into the surrounding space and directly into the host-cell cytoplasm. The effectors play pivotal roles from the onset of bacterial infection through to the establishment of the colonization of the intestinal epithelium, such as bacterial invasion, intracellular survival, subversion of the host immune defense response, and maintenance of the infectious foothold. These examples suggest that Shigella have evolved highly sophisticated infectious and intracellular strategies to establish replicative niches in the intestinal epithelium.
引用
收藏
页码:231 / 255
页数:25
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