期刊
CELLULAR MICROBIOLOGY
卷 10, 期 4, 页码 836-847出版社
WILEY
DOI: 10.1111/j.1462-5822.2007.01087.x
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资金
- NIAID NIH HHS [R01 AI046454-08, R21 AI067827, R21-AI67827, R01 AI049470, R01-AI49470, R01 AI046454, R01 AI049740-04] Funding Source: Medline
- NIDDK NIH HHS [P30DK-34928, P30 DK034928] Funding Source: Medline
- PHS HHS [R01-A146454] Funding Source: Medline
Enterohaemorrhagic Escherichia coli ( EHEC) O157: H7 induces filamentous actin-rich ` pedestals' on intestinal epithelial cells. Pedestal formation in vitro requires translocation of bacterial effectors into the host cell, including Tir, an EHEC receptor, and EspF(U), which increases the efficiency of actin assembly initiated by Tir. While inactivation of espF(U) does not alter colonization in two reservoir hosts, we utilized two disease models to explore the significance of EspF(U)-promoted actin pedestal formation. EHEC Delta espF(U) efficiently colonized the rabbit intestine during co-infection with wild-type EHEC, but co-infection studies on cultured cells suggested that EspFU produced by wild-type bacteria might have rescued the mutant. Significantly, EHEC Delta espF(U) by itself was fully capable of establishing colonization at 2 days post inoculation but unlike wild type, failed to expand in numbers in the caecum and colon by 7 days. In the gnotobiotic piglet model, an espF(U) deletion mutant appeared to generate actin pedestals with lower efficiency than wild type. Furthermore, aggregates of the mutant occupied a significantly smaller area of the intestinal epithelial surface than those of the wild type. Together, these findings suggest that, after initial EHEC colonization of the intestinal surface, EspF(U) may stabilize bacterial association with the epithelial cytoskeleton and promote expansion beyond initial sites of infection.
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