期刊
CELLULAR MICROBIOLOGY
卷 12, 期 8, 页码 1158-1173出版社
WILEY-HINDAWI
DOI: 10.1111/j.1462-5822.2010.01461.x
关键词
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资金
- National Institutes of Health [AI069116, HL084934, HL080098]
- Research Council of Norway Functional Genomics initiative (FUGE) through The Consortium of Advances Microbial Sciences and Technologies (CAMST)
- Research Council of Norway [166931, 152020, 183613]
- Department of Molecular Biosciences and Center for Molecular Biology and Neurosciences at the University of Oslo
P>Tissue damage predisposes humans to life-threatening disseminating infection by the opportunistic pathogen Pseudomonas aeruginosa. Bacterial adherence to host tissue is a critical first step in this infection process. It is well established that P. aeruginosa attachment to host cells involves type IV pili (TFP), which are retractile surface fibres. The molecular details of attachment and the identity of the bacterial adhesin and host receptor remain controversial. Using a mucosal epithelium model system derived from primary human tissue, we show that the pilus-associated protein PilY1 is required for bacterial adherence. We establish that P. aeruginosa preferentially binds to exposed basolateral host cell surfaces, providing a mechanistic explanation for opportunistic infection of damaged tissue. Further, we demonstrate that invasion and fulminant infection of intact host tissue requires the coordinated and mutually dependent action of multiple bacterial factors, including pilus fibre retraction and the host cell intoxication system, termed type III secretion. Our findings offer new and important insights into the complex interactions between a pathogen and its human host and provide compelling evidence that PilY1 serves as the principal P. aeruginosa adhesin for human tissue and that it specifically recognizes a host receptor localized or enriched on basolateral epithelial cell surfaces.
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