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Endotoxin plasma levels in patients suffering from alcoholic liver cirrhosis, are often elevated.However, unknown mechanisms prevent typical clinical symptoms of endotoxemia in most patients.Methods: We therefore investigated cytokine production and target cell desensitization in 27 patients with alcoholic liver cirrhosis (ALC) and 17 age matched healthy controls (C).Pro-and antiinflammatory cytokine production in plasma and whole blood cultures were measured by ELISA (Quantikine; Medgenix ).Target cell desensitization was determined by FACSanalysis of TNF receptor I on granulocytes and measurement of soluble E-Selectin in Plasma by ELISA (Quantikine).Results: LPS-induced TNF-ct release in whole blood cultures was slightly, but not significantly elevated (1936 vs. 781 pg/ml, n.s., ALC vs. C).Significantly elevated plasma levels of this cytokine (32.8 vs. 22.1 pg/ml, p<0.05) were measured.Significantly elevated plasma levels were also shown for slL-2 receptors (1480 vs. 410 U/ml, p<0.001),IL-6 (86,2 vs. 24,6 pg/ml, p<0,005) and IL-8 (424,5 vs. 109,2pg/ml, p<0,001) in patients plasma.However, elevated plasma levels were observed for IL-10 (5.9 vs. 1.9 pg/ml, ALC vs. C, p<0.05),TNF receptor I (3157 vs. 608 pg/ml, p<0,001) and II (3331 vs. 1066 pg/ml, p<0,001) as well as an upregulation of the LPS-induced ex vivo production of IL-10 (1.37 vs. 0.62 pg/ml, p<0.05) in cirrhotic patients.The parallel increase of antiinflammatory mediators in patients plasma seems to prevent an overwhelming proinflammatory response.Interestingly, we found a downregulation of TNF receptor I on patients granulocytes (4.8 vs. 7.1 mfi, ALC vs. C, p<0.05).This and only slightly elevated soluble E-Selectin levels (63,2 vs 40,0 ng/ml, p<0,05) in plasma give evidence for a diminished in vivo response to LPS and/or proinflammatory cytokines at the level of target cells.In conclusion, no downregulation of proinflammatory cytokine production could be observed in patients suffering from alcoholic liver cirrhosis.Clinical tolerance to chronic endotoxemia could be explained by an increased production of couterregulatory antiinflammatory cytokines and by target cell desensitization.These findings could explain the absence of typical inflammatory symptoms and the disturbance of reactivity against actute infections explaining the frequent infectious complications in patients with alcoholic liver cirrhosis.