Stress response decreases the interleukin-I beta-induced production of complement component C3 in human intestinal epithelial cells

Interleukin-1 beta (IL-1 beta) increases the production of complement compo nent C3 in enterocytes. Heat shock regulates the response to cytokines and other inflammatory mediators in various eel I types. We tested the hypothes is that the heat-shock response regulates IL-1 beta-induced C3 production i n the enterocyte. Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with sodium arsenite (10-500 mu M) for 1 h or subjected to hyperthermia (43 degrees C) for 1-4 h, and allowed to recover for 1 h. The cells were then treated with 1L-1 beta (0.5 ng/ml) for up to 24 h, wher eafter C3 levels were measured by ELISA and C3 mRNA by Northern blot analys is. Heat-shock protein of 72 kDa (hsp72) was determined by Western blot ana lysis. Treatment of the cells with sodium arsenite or subjecting them to hy perthermia induced the expression of hsp72. The IL-1 beta-induced expressio n of C3 mRNA and C3 production were down-regulated by hyperthermia and sodi um arsenite in a dose-dependent fashion. The results suggest that the stres s response induced by hyperthermia or sodium arsenite decreases IL-1 beta-i nduced C3 production in human enterocytes.