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Infection and Immunity, August 2008, p. 3390-3398, Vol. 76, No. 8
0019-9567/08/$08.00+0     doi:10.1128/IAI.01698-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Epidermal Growth Factor Inhibits Campylobacter jejuni-Induced Claudin-4 Disruption, Loss of Epithelial Barrier Function, and Escherichia coli Translocation{triangledown}

Jennifer M. Lamb-Rosteski,1 Lisa D. Kalischuk,1,2 G. Douglas Inglis,2 and Andre G. Buret1*

Department of Biological Sciences, Inflammation Research Network, University of Calgary, Calgary, Alberta, Canada,1 Agriculture and Agri-Food Canada, Lethbridge, Alberta, Canada2

Received 19 December 2007/ Returned for modification 8 February 2008/ Accepted 8 May 2008

Campylobacter jejuni is a leading cause of acute bacterial enteritis in humans. Poultry serves as a major reservoir of C. jejuni and is thought to act as a principal vehicle of transmission to humans. Epidermal growth factor (EGF) is a small amino acid peptide that exerts a broad range of activities on the intestinal epithelium. The aims of this study were to determine the effect of EGF on C. jejuni intestinal colonization in newly hatched chicks and to characterize its effects on C. jejuni-induced intestinal epithelial barrier disruption. White Leghorn chicks were treated with EGF daily, starting 1 day prior to C. jejuni infection, and were compared to control and C. jejuni-infected, EGF-treated chicks. Infected chicks shed C. jejuni in their feces throughout the study period. C. jejuni colonized the small intestine and cecum, disseminated to extraintestinal organs, and caused jejunal villus atrophy. EGF reduced jejunal colonization and dissemination of C. jejuni to the liver and spleen. In EGF-treated C. jejuni-infected chicks, villus height was not significantly different from that in untreated C. jejuni-infected chicks or controls. In vitro, C. jejuni attached to and invaded intestinal epithelial cells, disrupted tight junctional claudin-4, and increased transepithelial permeability. C. jejuni also promoted the translocation of noninvasive Escherichia coli C25. These C. jejuni-induced epithelial abnormalities were abolished by pretreatment with EGF, and the effect was dependent upon activation of the EGF receptor. These findings highlight EGF's ability to alter colonization of C. jejuni in the intestinal tract and to protect against pathogen-induced barrier defects.

* Corresponding author. Mailing address: Department of Biological Sciences, Inflammation Research Network, University of Calgary, 2500 University Dr. N.W., Calgary, Alberta T2N 1N4, Canada. Phone: (403) 220-2817. Fax: (403) 289-9311. E-mail: aburet{at}ucalgary.ca

{triangledown} Published ahead of print on 19 May 2008.

Editor: B. A. McCormick

Infection and Immunity, August 2008, p. 3390-3398, Vol. 76, No. 8
0019-9567/08/$08.00+0     doi:10.1128/IAI.01698-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Clark, J. A., Gan, H., Samocha, A. J., Fox, A. C., Buchman, T. G., Coopersmith, C. M. (2009). Enterocyte-specific epidermal growth factor prevents barrier dysfunction and improves mortality in murine peritonitis. Am. J. Physiol. Gastrointest. Liver Physiol. 297: G471-G479 [Abstract] [Full Text]  


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