EXPERIMENTAL COLITIS IN RATS INDUCES LOW-GRADE ENDOTOXINEMIA WITHOUT HEPATOBILIARY ABNORMALITIES

In three experimental models in rats, surgical construction of a self- filling blind loop (SFBL), trinitrobenzene sulfonic acid (TNB)-induced colitis, and the combination of SFBL and TNB, the hypothesis was stud ied that intestine-derived endotoxins play a role in the pathogenesis of hepatobiliary disorders in chronic inflammatory bowel disease (CIBD ). After eight weeks of treatment, a mild increase in portal and syste mic endotoxin levels and interleukin-6 concentrations was observed and the serum levels of alkaline phosphatase, bilirubin, and ALAT were on ly mildly increased in SFBL plus TNB rats. Histopathological examinati on of the liver showed hardly any abnormalities in all three rat model s. These results show that low-grade portal and systemic endotoxinemia in rats, induced by bacterial overgrowth and/or chemical colitis, is not able to induce hepatobiliary alterations. To exclude definitively a possible role for portal endotoxinemia in the pathogenesis of CIBD-a ssociated hepatobiliary abnormalities, however, an adequate animal mod el for CIBD is urgently needed.