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Infection and Immunity, November 1999, p. 5938-5945, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Shiga Toxin-Producing Escherichia coli Can Impair T84 Cell Structure and Function without Inducing Attaching/Effacing Lesions

Zhe Li,1 Elizabeth Elliott,2 Jacqueline Payne,2 Jacqui Isaacs,3 Peter Gunning,4 and Edward V. O'loughlin1,*

Intestinal Disease Research Unit1 and Oncology Research Units,4 Royal Alexandra Hospital for Children, Westmead, and The Department of Paediatrics and Child Health2 and Electron Microscopy Unit,3 University of Sydney, Sydney, New South Wales 2124, Australia

Received 31 December 1998/Returned for modification 9 March 1999/Accepted 23 July 1999

Enteropathogenic Escherichia coli (EPEC) intimately adhere to epithelial cells producing cytoskeletal rearrangement with typical attaching and effacing lesions and altered epithelial barrier and transport function. Since EPEC and Shiga toxin-producing E. coli (STEC) share similar genes in the "locus for enterocyte effacement" (LEE) thought to cause these changes, it has been assumed that STEC shares similar pathogenic mechanisms with EPEC. The aims of this study were to compare the effects of EPEC and STEC on bacterial-epithelial interactions and to examine changes in epithelial function. T84 monolayers were infected with STEC O157:H7 (wild strain EDL 933 or non-toxin-producing strain 85/170), EPEC (strain E2348/69), or HB101 (nonpathogenic) and studied at various times after infection. EPEC bound more avidly than EDL 933, but both strains exhibited greater binding than HB101. Attaching and effacing lesions and severe disruption to the actin cytoskeleton were observed in EPEC by 3 h postinfection but not in EDL 933 or HB101 at any time point. EPEC and EDL 933 increased monolayer permeability to [3H]mannitol 5- to 10-fold. In contrast to EPEC, EDL 933 completely abolished secretagogue-stimulated anion secretion as assessed under voltage clamp conditions in Ussing chambers. Several other STEC strains induced changes similar to those of EDL 933. In conclusion, STEC impairs epithelial barrier function and ion transport without causing major disruption to the actin cytoskeleton. Pathogenic factors other than products of LEE may be operant in STEC.

* Corresponding author. Mailing address: Department of Gastroenterology, Royal Alexandra Hospital for Children, Westmead, NSW 2124, Australia. Phone: 61-2-9845-3994. Fax: 61-2-9845-3970. E-mail: tedo{at}nch.edu.au.

Infection and Immunity, November 1999, p. 5938-5945, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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