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Infection and Immunity, November 2001, p. 7152-7158, Vol. 69, No. 11
Research Institute, Hospital for Sick
Children, Departments of Paediatrics and Laboratory Medicine & Pathobiology, University of Toronto, Toronto,
Ontario,1 and Department of
Pharmacology, University of Calgary, Calgary,
Alberta,2 Canada
Received 18 January 2001/Returned for modification 16 March
2001/Accepted 1 August 2001
Enteropathogenic Escherichia coli (EPEC) and Shiga
toxin-producing E. coli (STEC) induce cytoskeletal changes
in infected epithelial cells. To further characterize host cytosolic
responses to infection, a series of specific cell-signaling inhibitors
were employed. Initial bacterial adhesion to HEp-2 epithelial cells was
not reduced, whereas
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.11.7152-7158.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Inhibition of Attaching and Effacing Lesion
Formation following Enteropathogenic Escherichia coli
and Shiga Toxin-Producing E. coli Infection
-actinin accumulation in infected cells was
blocked by a phosphoinositide-specific phospholipase C inhibitor (ET-18-OCH3), phosphoinositide 3-kinase inhibitors
(wortmannin and LY294002), and a 5-lipoxygenase inhibitor,
nordihydroguaretic acid. A cyclooxygenase-2 inhibitor (NS-398),
however, did not block
-actinin reorganization in response to EPEC
and STEC infections. Understanding signal transduction responses to
enteric pathogens could provide the basis for the development of novel
therapeutic strategies.
*
Corresponding author. Mailing address: Division of
Gastroenterology and Nutrition, Room 8409, Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G 1X8, Canada. Phone: (416)
813-7734. Fax: (416) 813-6531. E-mail:
sherman{at}sickkids.on.ca.
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