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Endotoxin-induced cytokine release from whole blood - similarities between monocyte dysfunction in septic disease and during postoperative acute phase response

Department of General Surgery, University of Ulm, Ulm, Germany

E. Bölke

Department of General Surgery, University of Ulm, Ulm, Germany

M. Seidelmann

Department of General Surgery, University of Ulm, Ulm, Germany

C. Vasilescu

Department of General Surgery, University of Ulm, Ulm, Germany

H.G. Beger

Department of General Surgery, University of Ulm, Ulm, Germany

Plasma levels of endotoxin, TNF, interleukin-1β (IL-1β), and interleukin-6 (IL-6) as well as the endotoxin-induced release of these cytokines from whole blood were determined in 20 patients after elective aseptic surgery and eight patients suffering from septic disease. Blood samples were drawn before surgery as well as once daily over 7 days postoperatively. Endotoxin plasma levels increased on the day of the operation from 0.025 ± 0.005 EU/ml to 0.099 ± 0.022 EU/ml and remained elevated for 1 day. No changes were noted in the plasma levels of TNF and IL-1. Levels of IL-6 increased to 198 ± 52 pg/ml on the day of the operation, while the release of TNF and IL-6 markedly declined after whole blood was stimulated with endotoxin. The difference between basal and stimulated TNF values amounted to 505 ± 129 pg/ml preoperatively and 132 ± 41 pg/ml after the operation and 297 ± 28 pg/ml and 137 ± 43 pg/ml for IL-6. From the second day of the postoperative period onwards, the endotoxin-induced release of IL-6 was higher than the preoperative values. The results of whole blood stimulation in patients with sepsis were similar to those achieved directly after elective surgery. The cytokine release of TNF, IL-1β, and IL-6 was reduced. We conclude that, during the early aseptic acute phase reaction, the changes in the functioning of monocytes resemble - qualitatively - those occurring during septic disease, and that this may be related to endotoxemia originating in the gastrointestinal tract.

Journal of Endotoxin Research, Vol. 4, No. 1, 17-24 (1997)
DOI: 10.1177/096805199700400103


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