The iinate and acquired immune systems are both implicarted in the etiology of Inflammatory Bowel Disease (IBD) in addition to the genetic predisposition, the environmental factors and the intestinal flora covering the mucosa. A defect in the mucous covering will lead to an invasion of pathogens and stimulation of the immuune response with aberrations of mucin 2, the major mucin of the mucous layer. Aim: this study aims to assess the modulation of colonic MUC 2 and MUC 3 in a arat model of IBD induced by a combination of iodoacetamide and enteropatogenic E. Coli. Methods: 78 sprague-Dawley female rats were divided into 4 groups. Each group was subjeceted, on a basis, to a rectal injection of 1% methylcellulose (MC), the veicle, or saturated enteropathogenic E. coli bacterial suspension, or 3% iodoacetamide (IA) in 1% MC, or 3% IA followed by E. Coli infection 48 hours later. Biopsies of the colon were obtained for light microscopy and indirect immunofluorescence using a monoclonal primary antibody MUC 2 and MUC 3. Colonic mucosal scrapings were also use dfor RNA extraction and running for real-time PCR usong MUC 2 and MUC 3 primers. Results: Under light microscopy, the histological sections revealed severe colonic tissue damage in the IA and IA + B groups throughout the experiment. Conclusions: this induuced IBD model succeeded in the arousal and maintanence of IBD for a 2-months period. this inflammation lead to a clear mucosal tissue damage and disruption of the mucosal barrier, togheter with a decreased expression of MUC 2, both on the protein and the RNA levels, whereas MUC 3 expression was not significantly altered.
|Number of pages||2|
|Publication status||Published - 2016|