Stress response decreases the interleukin-1beta-induced production of complement component C3 in human intestinal epithelial cells.

Moon R, Pritts TA, Parikh AA, Fischer JE, Salzman AL, Ryan M, Wong HR, Hasselgren PO
Clin Sci (Lond). 1999 97 (3): 331-7

PMID: 10464058

Interleukin-1beta (IL-1beta) increases the production of complement component C3 in enterocytes. Heat shock regulates the response to cytokines and other inflammatory mediators in various cell types. We tested the hypothesis that the heat-shock response regulates IL-1beta-induced C3 production in the enterocyte. Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with sodium arsenite (10-500 microM) 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 IL-1beta (0.5 ng/ml) for up to 24 h, whereafter C3 levels were measured by ELISA and C3 mRNA by Northern blot analysis. Heat-shock protein of 72 kDa (hsp72) was determined by Western blot analysis. Treatment of the cells with sodium arsenite or subjecting them to hyperthermia induced the expression of hsp72. The IL-1beta-induced expression of C3 mRNA and C3 production were down-regulated by hyperthermia and sodium arsenite in a dose-dependent fashion. The results suggest that the stress response induced by hyperthermia or sodium arsenite decreases IL-1beta-induced C3 production in human enterocytes.

MeSH Terms (16)

Arsenites Cell Line Complement C3 Dose-Response Relationship, Immunologic Down-Regulation Epithelial Cells Heat-Shock Proteins Heat-Shock Response Hot Temperature HSP72 Heat-Shock Proteins Humans Interleukin-1 Intestinal Mucosa RNA, Messenger Sodium Compounds Sulfhydryl Reagents

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