THE ROLE OF INTESTINAL BACTERIA, BACTERIAL TRANSLOCATION AND ENDOTOXIN IN DEXTRAN SODIUM SULFATE-INDUCED COLITIS IN THE MOUSE

Experimental inflammation of the large intestine can be induced in mic e by oral administration of dextran sodium sulphate (DSS) given in the drinking water. This inflammation has been considered to require the presence of a normal microbiota. We have earlier shown that germ-free (GF) mice are susceptible to DSS-induced intestinal inflammation. To f urther investigate the relative importance of bacteria in this model w e induced DSS-intestinal inflammation in GF mice, in mice with a restr icted microbiota, and in mice with a conventional microbiota. In addit ion we used mice which are resistant to endotoxin. It was shown that t he intestinal inflammation in GF mice and conventional bacteria associ ated mice had a similar histological appearance and anatomical localis ation. In mice with a restricted microbiota, endotoxin measurements of serum samples showed that varying endotoxin levels could be found in healthy animals as well as in animals with DSS-induced intestinal infl ammation. Bacteriological investigations of organs such as the lung, l iver, spleen, mesenterial lymph nodes and blood were performed and no bacteria were found in healthy mice. In diseased mice varying amounts of bacteria were found but did not conform to the mortality in these m ice. The endotoxin receptor-deficient C3H/HeJ mice given DSS showed th e same mortality as conventional C3H/HeN mice. It was concluded that n either bacterial translocation from the intestine nor systemic endotox in has a crucial role in the mortality seen in severe cases of DSS-ind uced intestinal inflammation.