Cellular pathology of experimental colitis induced by trinitrobenzenesulphonic acid (TNBS): protective effects of recombinant human interleukin-11.

The objective of this study was to elucidate colonic mucosal ultrastructural effects of trinitrobenzene-sulphonic acid (TNBS) with and without co-administration of recombinant human interleukin-11 (rhIL-11). Using a standard colitis model (ir alcoholic TNBS), rats were sacrificed at 3~14 days after TNBS. Co-administration of rhIL-11 (100, 300 or 1000 mug/kg sc) was given for protection, and controls received saline or alcohol ir, or rhIL-11 sc alone. Transmission electron microscopy revealed that early TNBS-induced cytopathology was primarily in absorptive cells, changes which occurred prior to goblet cell damage. Progressive cellular changes included vacuolization and increased multivesicular bodies in cell apices, disconfiguration of microvilli, enlarged Golgi apparatuses, enlargement of basal inter-cellular spaces, and eventual desquamation of epithelium and apical bursting.Organelle damage preceded surface changes and resembled ultrastructural changes reported for human ulcerative colitis. The principal effect of rhIL-11 was apparent massive release of mucus from goblet cells, filling the colonic crypts, and suggesting a mode of its protection.