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Infection and Immunity, February 2005, p. 1161-1170, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.1161-1170.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mouse Model of Enteropathogenic Escherichia coli Infection

Suzana D. Savkovic,1* Jennilee Villanueva,1 Jerrold R. Turner,2 Kristina A. Matkowskyj,1 and Gail Hecht1

Section of Digestive and Liver Diseases, Department of Medicine, University of Illinois, West Side VA Medical Center,1 Department of Pathology, The University of Chicago, Chicago, Illinois2

Received 30 April 2004/ Returned for modification 9 June 2004/ Accepted 30 September 2004

Enteropathogenic Escherichia coli (EPEC) is an important cause of diarrhea in humans. EPEC infection of cultured intestinal epithelial cells induces attaching and effacing (A/E) lesions, alters intestinal ion transport, increases paracellular permeability, and stimulates inflammation. The lack of a small-animal model has restricted in vivo studies examining EPEC-host interactions. The aim of this study was to characterize the C57BL/6J mouse as a model of EPEC infection. We have shown that EPEC can adhere to and colonize the intestinal epithelium of C57BL/6J mice. Animal weight and water intake were not altered during 10 days of EPEC infection. The proximal colon of infected mice contained semisolid stool, with stool pellets forming only in the distal colon. In contrast, the entire colon of control mice contained formed stool. Microvillous effacement and actin rearrangement, characteristic of A/E lesions, were seen in the intestine of infected mice but not control mice. Histological assessment revealed increased numbers of lamina propria neutrophils with occasional crypt abscesses, intraepithelial lymphocytes, and goblet cells in the intestine of EPEC-infected mice. Altogether, these data suggest that the C57BL/6J mouse is susceptible to infection by EPEC and will provide a suitable in vivo model for studying the consequences of EPEC infection.

* Corresponding author. Mailing address: Section of Digestive and Liver Diseases, Department of Medicine, University of Illinois, 840 South Wood St., CSB Room 706 (m/c 716), Chicago, IL 60612. Phone: (312) 355-4133. Fax: (312) 996-5103. E-mail: sdsavkov{at}uic.edu.

Editor: J. T. Barbieri

Infection and Immunity, February 2005, p. 1161-1170, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.1161-1170.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Guttman, J. A., Samji, F. N., Li, Y., Vogl, A. W., Finlay, B. B. (2006). Evidence that Tight Junctions Are Disrupted Due to Intimate Bacterial Contact and Not Inflammation during Attaching and Effacing Pathogen Infection In Vivo. Infect. Immun. 74: 6075-6084 [Abstract] [Full Text]  
  • Sharma, R., Tesfay, S., Tomson, F. L., Kanteti, R. P., Viswanathan, V. K., Hecht, G. (2006). Balance of bacterial pro- and anti-inflammatory mediators dictates net effect of enteropathogenic Escherichia coli on intestinal epithelial cells. Am. J. Physiol. Gastrointest. Liver Physiol. 290: G685-G694 [Abstract] [Full Text]  


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