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December 1994

Endotoxin Stimulates Interleukin-6 Production in Intestinal Epithelial CellsA Synergistic Effect With Prostaglandin E2

Author Affiliations

From the Department of Surgery, University of Cincinnati Medical Center, and the Shriners Burn Institute, Cincinnati, Ohio.

Arch Surg. 1994;129(12):1290-1295. doi:10.1001/archsurg.1994.01420360080010

Objective:  To test the hypothesis that endotoxin stimulates the release of interleukin-6 (IL-6) from intestinal epithelial cells and that this effect of endotoxin is regulated by prostaglandin E2 (PGE2).

Design:  A rat intestinal crypt cell line, IEC-6, was cultured in the presence of lipopolysaccharide (LPS), 0.1 to 1.0 μg/mL, and/or PGE2, 1 μmol/L. In other experiments, indomethacin, 20 μmol/L, was added to LPS-treated cells to block the effects of prostaglandins. Control wells contained medium alone. Levels of IL-6 were determined by the B9 murine hybridoma bioassay. Polymerase chain reaction was performed on RNA from control and LPS-treated cells to examine IL-6 message.

Results:  Lipopolysaccharide and PGE2 induced IL-6 release from IEC-6 cells in a dose- and time-dependent fashion, and the substances interacted synergistically. Addition of indomethacin blunted the effect of endotoxin on IL-6 production, consistent with a stimulatory role of PGE2. Polymerase chain reaction demonstrated increased IL-6 messenger RNA in endotoxin-treated cells.

Conclusions:  Endotoxin and PGE2 stimulate IL-6 production in IEC-6 cells and interact synergistically. The endotoxin-stimulated IL-6 release may be regulated at the transcriptional level.(Arch Surg. 1994;129:1290-1295)