Report

Role of Bacterial Intimin in Colonic Hyperplasia and Inflammation

Science  23 Jul 1999:
Vol. 285, Issue 5427, pp. 588-591
DOI: 10.1126/science.285.5427.588

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Abstract

Enteropathogenic Escherichia coli (EPEC) cells adhere to gut epithelial cells through intimin α: the ligand for a bacterially derived epithelial transmembrane protein called the translocated intimin receptor. Citrobacter rodentium colonizes the mouse colon in a similar fashion and uses a different intimin: intimin β. Intimin α was found to costimulate submitogenic signals through the T cell receptor. Dead intimin β+ C. rodentium, intimin α–transfected C. rodentium or E. colistrain K12, and EPEC induced mucosal hyperplasia identical to that caused by C. rodentium live infection, as well as a massive T helper cell–type 1 immune response in the colonic mucosa. Mutation of cysteine-937 of intimin to alanine reduced costimulatory activity in vitro and prevented immunopathology in vivo. The mucosal changes elicited by C. rodentium were interferon-γ–dependent. Immunopathology induced by intimin enables the bacteria to promote conditions that are favorable for increased microbial colonization.

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