Interleukin 10‐deficient colitis: new similarities to human inflammatory bowel disease

Background: Interleukin (IL) 10 is a potent anti-inflammatory cytokine. Disruption of the IL-I0 gene in C57/Black6 rnice results in enterocolitis in the presence of intestinal bacteria. This study investigated gut mucosal barrier function sequentially during the development of colitis in this modelo Methods: Animals were bred in specific pathogen-free conditions and transferred to convencional housing at 4weeks. Mice were evaluated at 6,8,10,12,14 and 15weeks ofage. Barrler function was assessed by measuring intestinal permeability and antibody response to systernic endotoxaernia (antibody to the core glycolipid region of lipopolysaccharide; EndoCAb). Colons were harvested and a histological injury score (IllS) was calculated. Results: The ms increased progressively until 12 weeks, with an associated increase in intestinal permeability, and irnmunoglobulin (Ig) M and IgG EndoCAb. The ms correlated positively with both intestinal permeability and IgM and IgG EndoCAb. Intestinal permeability showed a positive correlation with EndoCAb. Conclusion: n.-IO knockout rnice develop coli*1h an associated disturbance in gut mucosal barrier function, as measured by increased ~ermeability and endotoxaernia. The colitis found in the IL-I0 knockout mouse