C57BL/6 and Congenic Interleukin-10-Deficient Mice Can Serve as Models ofCampylobacter jejuniColonization and Enteritis

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Abstract
Campylobacter jejuniis a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized thatC. jejuni11168 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 experienceC. jejuni11168-mediated clinical signs and pathology. Individually housed mice were challenged orally withC. jejuni11168, 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 ofC. jejuni11168-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 withC. jejuni11168, 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 106CFU produced significant disease and pathological lesions similar to responses seen in humans. Immunohistochemical staining demonstratedC. jejuniantigens within gastrointestinal tissues of infected mice. Significant anti-C. jejuniplasma 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 byC. jejuni11168 is necessary but not sufficient for the development of enteritis and that C57BL/6 IL-10−/−mice can serve as models for the study ofC. jejunienteritis in humans.