COLITIS AND COLONIC MUCOSAL BARRIER DYSFUNCTION

Trauma, infection, neoplasia, and inflammation can all disrupt the int act intestinal mucosal barrier to intraluminal bacteria and bacterial antigens. This study investigated the relation between colonic inflamm ation and colonic mucosal barrier function in three experimental model s of colitis. There were significantly increased systemic endotoxin co ncentrations in rats with acetic acid (7.5 (1.7-119.5) pg/ml), ethanol (13.7 (0-111.2) pg/ml), and hapten induced (14.4 (5-31.1) compared wi th saline (0-13.7) pg/ml). Data expressed as median (range). There wer e significant correlations between the systemic endotoxin concentratio n and both the severity of colitis and of illness in acetic acid induc ed colitis. A significant increase in colonic permeability to C-14-pol yethylene glycol was shown in rats with acetic acid (3.42 (1.36-5.63)% ) and hapten induced colitis (2.86 (1.03-8.10)%) compared with saline controls (1.20 (0.67-1.36)%). Data expressed as median (range) of perc entage of the intracolonic bolus excreted in urine. There was a signif icant positive correlation between the severity of colitis and % colon ic permeability to C-14-polyethylene glycol. This and other studies pr ovide evidence that mucosal barrier dysfunction is a feature of coliti s irrespective of aetiology or species. Such barrier dysfunction may b e responsible for the systemic inflammatory response complications see n in patients inflammatory bowel disease.