Interleukin-6 mediates host defense responses induced by abdominal surgery

Abstract

Background: Cytokines have been implicated as pivotal mediators of the host defense reaction. In patients undergoing surgery we investigated the relationship between such mediators and postoperative host defense responses.

Methods: Tumor necrosis factor (TNF) was determined with an immunoradiometric assay, interleukin (IL)-6 by a B9-cell bioassay, and endotoxin by a chromogenic limulus lysate assay. C-reactive protein, alpha 1-antitrypsin, and alpha 2-macroglobulin were quantified by nephelometric assay.

Results: In 19 consecutive patients undergoing pancreaticoduodenectomy, a large increase in portal, and a significantly lower increase in peripheral, IL-6 levels was observed. No significant increase in TNF levels was noted. Fever developed in 16 patients within 24 hours (84%). The highest peripheral IL-6 levels correlated logarithmically (R = 0.59; p = 0.0039) with the peak body temperatures. C-reactive protein levels correlated with IL-6 levels (R = 0.49; p = 0.020). Increased IL-6 levels were observed in all nine patients undergoing either hemihepatectomy, breast reduction, or extensive breast reconstruction; however, only patients undergoing hemihepatectomy had endotoxemia.

Conclusions: We conclude that abdominal surgery causes acute release of IL-6, but not TNF, in the portal circulation. IL-6 seems to be a major endogenous mediator of fever and the acute-phase response. The presence of endotoxin might be synergistic but is not obligatory for the host defense response after surgical trauma.