Redistribution of Tight Junction Proteins During EPEC Infection In Vivo
Enteropathogenic Escherichia coli (EPEC) is a leading cause of diarrhea among infants. Tight junction plays a vital role in intestinal paracellular permeability by forming physical intercellular barriers in epithelial cells. However, the impact of this enteric pathogen on tight junctions in vivo has not been fully investigated. In the present study, the alterations in tight junctions following EPEC infection in vivo were investigated. Western blot analysis revealed that the tight junction proteins, occludin and claudin-1, were displaced from tight junction membrane microdomains to Triton X-100 soluble fractions after EPEC infection. Changes in intestinal paracellular permeability were determined using the molecular tracer biotin, which was observed to penetrate the epithelia and extended into the lamina propria, indicating disruption in tight junction barrier function. Our results suggested that redistribution of tight junction proteins plays an important role in the disruption of epithelial barrier function induced by EPEC infection, which may provide new insight into the pathogenesis of diarrhea caused by EPEC.
KEY WORDSenteropathogenic E. coli tight junction claudins occludin barrier function
This work was supported by the Key Project of National Natural Science Foundation in China (30830098), the National Basic Research Program (973 Program) in China (Nos. 2007CB513005 and 2009CB522405), the National Natural Science Foundation in China (81070375), the Scientific Research Fund in Jiangsu Province (BK2009317), and the National Key Project of Scientific and Technical Supporting Programs funded by the Ministry of Science & Technology of China (2008BAI60B06).
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