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Infection and Immunity, March 2007, p. 1099-1115, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.00833-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

C57BL/6 and Congenic Interleukin-10-Deficient Mice Can Serve as Models of Campylobacter jejuni Colonization and Enteritis{triangledown}

L. S. Mansfield,1,2,3* J. A. Bell,1,4 D. L. Wilson,1,4 A. J. Murphy,1,2,3 H. M. Elsheikha,1,3,6,{dagger} V. A. K. Rathinam,1,2,3 B. R. Fierro,1,2,3 J. E. Linz,1,2,4 and V. B. Young1,2,5

National Food Safety and Toxicology Center,1 Department of Microbiology and Molecular Genetics,2 Department of Large Animal Clinical Sciences,3 Department of Food Science and Human Nutrition,4 Department of Internal Medicine/Infectious Diseases Division, Michigan State University, East Lansing, Michigan,5 Department of Parasitology, College of Veterinary Medicine, Mansoura University, Mansoura 35516, Egypt6

Received 23 May 2006/ Returned for modification 25 July 2006/ Accepted 2 November 2006

Campylobacter jejuni is a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized that C. jejuni 11168 colonizes the gastrointestinal tract of both C57BL/6 mice and congenic C57BL/6 interleukin-10-deficient (IL-10–/–) mice and that C57BL/6 IL-10–/– mice experience C. jejuni 11168-mediated clinical signs and pathology. Individually housed mice were challenged orally with C. jejuni 11168, and the course of infection was monitored by clinical examination, bacterial culture, C. jejuni-specific PCR, gross pathology, histopathology, immunohistochemistry, and anti-C. jejuni-specific serology. Ceca of C. jejuni 11168-infected mice were colonized at high rates: ceca of 50/50 wild-type mice and 168/170 IL-10–/– mice were colonized. In a range from 2 to 35 days after infection with C. jejuni 11168, C57BL/6 IL-10–/– mice developed severe typhlocolitis best evaluated at the ileocecocolic junction. Rates of colonization and enteritis did not differ between male and female mice. A dose-response experiment showed that as little as 106 CFU produced significant disease and pathological lesions similar to responses seen in humans. Immunohistochemical staining demonstrated C. jejuni antigens within gastrointestinal tissues of infected mice. Significant anti-C. jejuni plasma immunoglobulin levels developed by day 28 after infection in both wild-type and IL-10-deficient animals; antibodies were predominantly T-helper-cell 1 (Th1)-associated subtypes. These results indicate that the colonization of the mouse gastrointestinal tract by C. jejuni 11168 is necessary but not sufficient for the development of enteritis and that C57BL/6 IL-10–/– mice can serve as models for the study of C. jejuni enteritis in humans.

* Corresponding author. Mailing address: 181 Food Safety Building, Michigan State University, East Lansing, MI 48824. Phone: (517) 432-3100, ext. 119. Fax: (517) 432-2310. E-mail: mansfie4{at}cvm.msu.edu.

{triangledown} Published ahead of print on 27 November 2006.

Editor: V. J. DiRita

{dagger} Present address: Division of Comparative Veterinary Medicine, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire LE12 5RD, United Kingdom.

Infection and Immunity, March 2007, p. 1099-1115, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.00833-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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