Mechanisms and consequences of bladder cell invasion by uropathogenic Escherichia coli

被引:107
作者
Dhakal, B. K. [1 ]
Kulesus, R. R. [1 ]
Mulvey, M. A. [1 ]
机构
[1] Univ Utah, Dept Pathol, Div Cell Biol & Immunol, Salt Lake City, UT 84112 USA
基金
美国国家卫生研究院;
关键词
Fimbriae; integrin; invasion; UPEC; UTI; uroplakin;
D O I
10.1111/j.1365-2362.2008.01986.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Strains of uropathogenic Escherichia coli (UPEC) are the major cause of urinary tract infections worldwide. Multiple studies over the past decade have called into question the dogmatic view that OPEC strains act as strictly extracellular pathogens. Rather, bacterial expression of filamentous adhesive organelles known as type 1 pili and Afa/Dr fibrils enable UPEC to invade host epithelial cells within the urinary tract. Entry into bladder epithelial cells provides UPEC with a protected niche where the bacteria can persist quiescently for long periods, unperturbed by host defences and protected from many antibiotic treatments. Alternately, internalized UPEC can rapidly multiply, forming large intracellular inclusions that can contain several thousand bacteria. Initial work aimed at defining the host and bacterial factors that modulate the entry, intracellular trafficking, and eventual resurgence of UPEC suggests a high degree of host-pathogen crosstalk. Targeted disruption of these processes may provide a novel means to prevent and treat recurrent, relapsing and chronic infections within the urinary tract.
引用
收藏
页码:2 / 11
页数:10
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