期刊
FEBS JOURNAL
卷 275, 期 23, 页码 6022-6032出版社
WILEY
DOI: 10.1111/j.1742-4658.2008.06731.x
关键词
enteropathogenic Escherichia coli; lipid raft; TER; tight junction; tight junction protein
资金
- National Basic Research Program (973 Program) in China [2007CB513005, 2009CB522405]
- National Natural Science Foundation in China [30830098, 30672061]
- Nanjing Military Command [06Z40]
- Military Scientific Research Fund [0603AM117]
- Deutscher Akademischer Austauschdienst Researcher Fellowship
Enteropathogenic Escherichia coli (EPEC) has been shown to disrupt the barrier function of host intestinal epithelial tissues through entering tight junctions. However, the mechanism by which this occurs remains poorly understood. In this study, we determined that EPEC invades host cells through tight junctions as it initiates infection. Immunofluorescence microscopy revealed redistribution of the tight-junction proteins occludin and ZO-1 from an intercellular to a cytoplasmic location after EPEC invasion. Flotillin-1 was recruited to sites of EPEC entry. EPEC entered host cells through tight-junction membrane microdomains. Tight-junction ultrastructure was disrupted following EPEC infection, accompanied by loss of barrier function. EPEC infection caused a time-dependent decrease in trans-epithelial electrical resistance. Subcellular fractionation using discontinuous sucrose density gradients demonstrated a decline in raft-associated occludin following exposure to EPEC. These results indicate the important role of host membrane tight-junction microdomains in EPEC invasion.
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