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Infection and Immunity, May 2008, p. 1858-1865, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.01688-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Type 2 Secretion Promotes Enterohemorrhagic Escherichia coli Adherence and Intestinal Colonization{triangledown}

Theresa D. Ho,{dagger} Brigid M. Davis, Jennifer M. Ritchie, and Matthew K. Waldor*

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

Received 18 December 2007/ Returned for modification 22 January 2008/ Accepted 20 February 2008

Enterohemorrhagic Escherichia coli (EHEC) is a noninvasive food-borne pathogen that colonizes the distal ileum and colon. Proteins encoded in the EHEC locus of enterocyte effacement (LEE) pathogenicity island are known to contribute to this 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 the Z2053 gene (designated adfO here), a gene located in a cryptic EHEC prophage, exhibits similarity to adherence and/or colonization factor genes found in several other enteric pathogens. An EHEC adfO mutant exhibited marked reductions 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 that the colonization of an etpC (T2SS) mutant was reduced ~5-fold. 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 thus show that EHEC pathogenicity depends on type 2 secretion as well as type 3 secretion.

* Corresponding author. Mailing address: Channing Laboratory, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115. Phone: (617) 525-4646. Fax: (617) 525-4660. E-mail: mwaldor{at}rics.bwh.harvard.edu

{triangledown} Published ahead of print on 3 March 2008.

Editor: A. J. Bäumler

{dagger} Present address: Department of Microbiology, The University of Iowa, Iowa City, IA 52242.

Infection and Immunity, May 2008, p. 1858-1865, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.01688-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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