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

Campylobacter jejuni is a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized thatC. 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 experienceC. jejuni 11168-mediated clinical signs and pathology. Individually housed mice were challenged orally withC. 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 ofC. 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 withC. 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 demonstratedC. 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 byC. 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 ofC. jejuni enteritis in humans.