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

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, V. A. K. Rathinam,^1,2,3 B. R. Fierro,^1,2,3 J. E. Linz,^1,2,4 and V. B. Young^1,2,5

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.

Published ahead of print on 27 November 2006.

Editor: V. J. DiRita

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.

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