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Infection and Immunity, February 2002, p. 945-952, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.945-952.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Intimin, Tir, and Shiga Toxin 1 Do Not Influence Enteropathogenic Responses to Shiga Toxin-Producing Escherichia coli in Bovine Ligated Intestinal Loops

Mark P. Stevens,1 Olivier Marchès,2 June Campbell,1 Veronika Huter,2 Gad Frankel,3 Alan D. Phillips,4 Eric Oswald,2 and Timothy S. Wallis1*

Division of Environmental Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire, RG20 7NN ,1 Department of Biochemistry, Imperial College of Science, TechnologyMedicine, London, SW7 2AZ,,3 and University Department of Paediatric Gastroenterology, Royal Free Hospital, London, NW3 2QG, United Kingdom,4 Unité Mixte de Microbiologie Moléculaire, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, 31076 Toulouse Cedex, France2

Received 10 August 2001/ Returned for modification 1 October 2001/ Accepted 23 October 2001

Shiga toxin-producing Escherchia coli (STEC) comprises a group of attaching and effacing (A/E) enteric pathogens of animals and humans. Natural and experimental infection of calves with STEC may result in acute enteritis or subclinical infection, depending on serotype- and host-specific factors. To quantify intestinal secretory and inflammatory responses to STEC in the bovine intestine, serotypes that are associated with human disease (O103:H2 and O157:H7) were introduced into ligated mid-ileal loops in gnotobiotic and conventional calves, and fluid accumulation and recruitment of radiolabeled neutrophils were measured after 12 h. STEC serotype O103:H2, but not serotype O157:H7, elicited strong enteropathogenic responses. To determine if the inflammatory response to STEC O103:H2 in calves requires Shiga toxin 1 or intimate bacterial attachment to the intestinal epithelium, defined mutations were made in the stx1, eae, and tir genes. Our data indicate that some STEC induce intestinal inflammatory responses in calves by a mechanism that is independent of A/E-lesion formation, intimin, or Shiga toxin 1. This may have implications for strategies to reduce STEC carriage in cattle.

* Corresponding author. Mailing address: Division of Environmental Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire, RG20 7NN, United Kingdom. Phone: 44 1635 577230. Fax: 44 1635 577263. E-mail: timothy.wallis{at}bbsrc.ac.uk.

Editor: A. D. O'Brien

Infection and Immunity, February 2002, p. 945-952, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.945-952.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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