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Infect Immun, April 1998, p. 1688-1696, Vol. 66, No. 4
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Divergent Signal Transduction Responses to Infection with Attaching and Effacing Escherichia coli

Arif Ismaili,1,2 Elaine McWhirter,2,3 Michelle Y. C. Handelsman,2,3 James L. Brunton,2,3 and Philip M. Sherman1,2,4,*

Division of Gastroenterology and Nutrition, Research Institute, The Hospital for Sick Children,1 Samuel Lunenfeld Research Institute, Mount Sinai Hospital,3 and Departments of Pediatrics4 and Molecular and Medical Genetics,2 University of Toronto, Toronto, Ontario, Canada

Received 3 July 1997/Returned for modification 9 September 1997/Accepted 9 January 1998

Shiga toxin-producing Escherichia coli (STEC) O157:H7 is an attaching and effacing pathogen that causes hemorrhagic colitis and the hemolytic-uremic syndrome. Although this organism causes adhesion pedestals, the cellular signals responsible for the formation of these lesions have not been clearly defined. We have shown previously that STEC O157:H7 does not induce detectable tyrosine phosphorylation of host cell proteins upon binding to eukaryotic cells and is not internalized into nonphagocytic epithelial cells. In the present study, tyrosine-phosphorylated proteins were detected under adherent STEC O157:H7 when coincubated with the non-intimately adhering, intimin-deficient, enteropathogenic E. coli (EPEC) strain CVD206. The ability to be internalized into epithelial cells was also conferred on STEC O157:H7 when coincubated with CVD206 ([158 ± 21] % of control). Neither the ability to rearrange phosphotyrosine proteins nor that to be internalized into epithelial cells was evident following coincubation with another STEC O157:H7 strain or with the nonsignaling espB mutant of EPEC. E. coli JM101(pMH34/pSSS1C), which overproduces surface-localized O157 intimin, also rearranged tyrosine-phosphorylated and cytoskeletal proteins when coincubated with CVD206. In contrast, JM101(pMH34/pSSS1C) demonstrated rearrangement of cytoskeletal proteins, but not tyrosine-phosphorylated proteins, when coincubated with intimin-deficient STEC (strains CL8KO1 and CL15). These findings indicate that STEC O157:H7 forms adhesion pedestals by mechanisms that are distinct from those in attaching and effacing EPEC. Taken together, these findings point to diverging signal transduction responses to infection with attaching and effacing bacterial enteropathogens.

* Corresponding author. Mailing address: Division of Gastroenterology and Nutrition (Room 8411), The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada M5G 1X8. Phone: (416) 813-6185. Fax: (416) 813-6531. E-mail: sherman{at}sickkids.on.ca.




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