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Bacteria often express numerous virulence factors. These virulence factors make them successful pathogens, by e.g. mediating attachment to host cells and thereby facilitating persistence or invasion, or by contributing to the evasion of the host immune system to allow proliferation and spread within the host and in the environment. The site of first contact of Gram negative bacteria with the host is the bacterial outer membrane (OM). Consisting of an asymmetrical lipid bilayer with phospholipids forming the inner, and lipopolysaccharides forming the outer leaflet, the OM harbors numerous integral membrane proteins that are almost exclusively β-barrel proteins. One distinct family of OM β-barrel proteins strongly linked to bacterial virulence are the autotransporter (AT) proteins. During the last years huge progress has been made to better understand the mechanisms underlying the insertion of AT proteins into the OM and also AT function for interaction with the host. This review shortly summarizes our current knowledge about outer membrane protein (OMP) and more specifically AT biogenesis and function. We focused on the AT proteins that we haved studied in most detail: i.e. the Yersinia adhesin A (YadA) and invasin of Yersinia enterocolitica (Ye) as well as its homolog intimin (Int) expressed by enteropathogenic Escherichia coli. In addition, this review provides a short outlook about how we could possibly use this knowledge to fight infection.  相似文献   
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目的:研究周质伴侣蛋白SurA对伤寒沙门菌生物膜形成能力的影响及其潜在机制。方法:用前期构建的surA基因缺陷株、缺陷空载体株及缺陷回补株的生物膜实验,观察surA基因缺失对细菌生物膜形成能力的影响。通过实时定量聚合酶链式反应(quantitative real-time polymerase chain reaction, qRT-PCR)检测影响生物膜形成的几个关键基因在surA缺陷株及野生株中的表达差异,探索surA影响细菌生物膜形成的可能通路。通过电镜实验观察surA缺陷株及野生株的鞭毛表达情况。最后通过生物膜实验观察鞭毛缺失对生物膜形成的影响。结果:与野生株相比,surA缺陷株的生物膜形成能力显著下调,缺陷株里回补surA后,细菌的生物膜形成能力恢复到与野生株相当。与野生株相比,surA缺陷株中鞭毛相关基因的mRNA水平显著下调。电镜结果显示,与野生株相比,surA缺陷株的鞭毛表达数量显著减少。鞭毛缺失株(△flhD)几乎不形成生物膜。结论:伤寒沙门菌surA基因缺陷可能通过下调鞭毛基因表达来影响生物膜形成。  相似文献   
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