Superinfection with helicobacter hepaticus does not alter the natural course of colitis in IL-10 deficient mice

Abstract

IL-10 deficient mice (IL-10 -/-) spontaneously develop colitis when housed in microisolators (SPF housing). The severity and rate of disease onset is aggravated when these mice are maintained in conventional housing, suggesting that gastrointestinal flora contribute to the inflammation. Recent reports have implicated intestinal Helicobacter species in the development of colitis in immunodeficient mice. We investigated whether H. hepaticus infection can promote the development of colitis in IL-10 / mice. Clinical signs of colitis in SPF-housed IL-10 /mice on a C57BL/10 background (weight loss, blood in the stool) are observed at 12 weeks of age and histological inflammation (crypt abscesses, ulcerations, skip lesions, transmural infiltration, epithelial hyperplasia) is maximal at 18-20 weeks. IL-104were superinfected with 107 bacteria by oral gavage at 12 weeks of age and examined for occult blood in the feces, Helicobacter specific serum antibody titers and microscopic inflammation at 24 weeks. All naive and superinfected mice had evidence of fecal blood. Rectal prolapse was observed in 50% of the animals in both groups. Histological scoring for tissue damage and degree of inflammation demonstrated severe focal inflammation in all animals. No significant differences were noted between groups. These data demonstrate that superinfection with H. hepaticus does not increase the rate of disease onset, exacerbate the severity of inflammation, or modify the course of the colitis. It remains to be determined whether intestinal Helicobacter species play a role in the initiation or propagation Of colitis.