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Infect. Immun. doi:10.1128/IAI.01688-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Type 2 secretion promotes EHEC adherence and intestinal colonization

Channing Laboratory, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115

^* To whom correspondence should be addressed. Email: mwaldor{at}rics.bwh.harvard.edu.

	Abstract

Enterohemorrhagic Escherichia coli (EHEC) is a non invasive food-borne pathogen that colonizes the distal ileum and colon. Proteins encoded in the EHEC LEE pathogenicity island are known to contribute to the pathogen's adherence to epithelial cells and intestinal colonization. The role of non-LEE encoded proteins in these processes is not as clear. We found that z2053 (here renamed adfO), a gene located in a cryptic EHEC prophage, bears similarity to adherence and/or colonization factors found in several other enteric pathogens. An EHEC adfO mutant exhibited a marked reduction in adherence to HeLa cells and in the secretion of several proteins into the supernatant. YodA, one of these secreted proteins, was found to be a substrate of the EHEC pO157-encoded type 2 secretion system (T2SS). Both the T2SS and YodA proved to be essential for EHEC adherence to cultured HeLa cell monolayers. Using an infant rabbit model of infection, we found that the adfO mutation did not affect colonization but the etpC (T2SS) mutant had an 5-fold reduction in colonization. A strain deficient in YodA had a more severe colonization defect; however, this strain also exhibited a growth defect in vitro. Overall, our findings indicate that the pO157-encoded T2SS contributes to EHEC adherence and intestinal colonization and thereby reveal that EHEC pathogenicity depends upon type 2 as well as type 3 secretion.