Interleukin 1 beta is expressed predominantly by enterocytes in experimental colitis. The cytokine interleukin 1 beta is an important mediator of inflammatory processes capable of inducing eicosanoid production, T-cell activation, and increased vascular permeability. In this study, in situ hybridization techniques were used to delineate the kinetics and cellular source of induced interleukin 1 beta in acute experimental colitis. The induction of interleukin 1 beta messenger RNA was an early phenomenon and occurred predominantly in undifferentiated cells located in the basal part of the mucosal crypts but not in differentiated enterocytes. The undifferentiated enterocytes retained the messenger RNA during differentiation and migration to more apical parts of the crypts. These results suggest that induction of interleukin 1 beta messenger RNA in enterocytes is causally related to the subsequent inflammatory changes seen in acute experimental colitis. 