• LPS-Inactivation;
  • Cytokines;
  • IL-10;
  • sICAM;
  • sCD14

Background: Chronic alcohol ingestion leads to endoto-emia which is believed to play an important role in the pathogenesis of alcoholic liver disease (ALD). The purpose of this study was to determine if chronic ethanol consumption, in addition to affecting plasma endoto-in and cytokines, also affects the endoto-in-neutralizing capacity (ENC), sCD14, and sICAM-1, in patients with ALD. A second aim was to identify correlations between these latter parameters, endoto-in, and cytokines, especially IL-10.

Methods: Hospitalized patients with various degrees of ALD (n= 59), and 20 healthy volunteers were studied. Plasma endotoxin and ENC were determined using our kinetic Limulus amebocyte lysate test. Cytokines, sCD14, and sICAM-1 were measured by enzyme-linked immunosorbent assay.

Results: Patients with ALD e-hibited a mild endoto-emia (p < 0.01) and a marked decrease in ENC (p < 0.0002). TNF-α (p < 0.05), IL-6 (p < 0.0001), sICAM (p < 0.005), and sCD14 (p < 0.0005) were significantly elevated in all patients with ALD, and IL-10 (p < 0.05) in patients with cirrhotic ALD. With the exception of IL-10, the cytokines correlated with each other and with sICAM-1. No correlations occurred between endotoxin, ENC, and sCD14, and between these and the cytokines and sICAM-1. Elevated levels of endotoxin correlate with acute excessive alcohol ingestion. No gender differences were observed.

Conclusions: Acute alcohol into-ication rather than severe ALD results in significant endoto-emia. The limited capacity of plasma to neutralize endoto-in in liver injury seems to be an important factor in ALD which may be responsible for the release of endoto-in-induced mediators, such as cytokines, as well as s-ICAM-1, that are relevant in the pathogenesis of ALD.