In a model of bacterial-induced colitis, C3H mice develop catarrhal cecitis following infection with Serpulina hyodyseweriae. Disease is localized to the mucosal surface and lamina propria. Histopathological lesions include mucosal edema, epithelial erosion, crypt epithelial cell hyperplasia, and inflammatory cell infiltration into the lamina propria. We have utilized mAb against leukocyte integrins CD18 (fc) or CD29 (βi) to affect the development of lesions induced by S. hyodysenteriae. Mice were treated with either CD 18 or CD29 mAb prior to and/or following infection. Three days after infection, mice were necropsied and cecal lesions were assessed on the basis of intraluminal mucus and/or cecal atrophy. Macroscopic lesions in treated mice were less severe than in IgG-treated mice. Histological evaluation of cecal tissue corroborated the macroscopic observations in that lesions were less severe in mice treated with either mAb. Administration of mAb significantly reduced leukocyte infiltration into the mucosa, and there was little evidence of edema or epithelial damage. However, mice treated with either mAb exhibited the characteristic increase in the depth of cecal crypts following infection. These observations were in contrast to the severe inflammation observed in tissues of infected mice treated with IgG antibody. The results indicate that we can affect the development of intestinal lesions and begin to examine specific cell types responsible for the induction and/or maintenance of colitis.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology