Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 107, Issue 5, Pages 621-629Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI11138
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Funding
- NIAID NIH HHS [R56 AI032074, AI-32074, R01 AI018000, R01 AI032074, R01 AI037606, AI-37606] Funding Source: Medline
- NIDDK NIH HHS [R01 DK050694, R56 DK050694] Funding Source: Medline
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The mechanisms by which enteropathogenic Escherichia coli (EPEC), an important cause of diarrhea among infants in developing countries, induce symptoms are not defined. EPEC have a type III secretion system required for characteristic attaching and effacing changes that modify the cytoskeleton and apical surface of host cells. Infection of polarized intestinal epithelial cell monolayers by EPEC leads to a loss of transepithelial electrical resistance, which also requires the type III secretion system. We demonstrate here that EspF, a protein chat is secreted by EPEC via the type III secretion system, is not required for quantitatively and qualitatively typical attaching and effacing lesion formation in intestinal epithelial cells. However, EspF is required in a dose-dependent fashion for the loss of transepithelial electrical resistance, for increased monolayer permeability, and for redistribution of the tight junction-associated protein occludin, Furthermore, the analysis of EPEC strains expressing EspF-adenylate cyclase fusion proteins indicates that EspF is translocated via the type III secretion system to the cytoplasm of host cells, a result: confirmed by immunofluorescence microscopy. These studies suggest a novel role for EspF as an effector pro rein that disrupts intestinal barrier function without involvement in attaching and effacing lesion formation.
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