Alcohol and Alcoholism Advance Access originally published online on August 2, 2004
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Alcohol & Alcoholism Vol. 39, No. 5, pp. 386-392, 2004
Alcohol & Alcoholism Vol. 39, No. 5 © Medical Council on Alcohol 2004; all rights reserved
CHRONIC ALCOHOLISM CAUSES DELETERIOUS CONDITIONING OF INNATE IMMUNITY
1 Department of Immunology, Medical Faculty, University of Greifswald, Greifswald, 2 Johanna-Odebrecht-Foundation, Evangelical Hospital Bethanien, Greifswald and 3 Institute of Bacteriology and Mycology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany
* Author to whom correspondence should be addressed at: Department of Immunology, Medical Faculty, University of Greifswald, Diagnostikzentrum/Sauerbruchstrasse, D-17487 Greifswald, Germany. Tel.: +49 3834 865454; Fax: +49 3834 865490; E-mail: frankj{at}uni-greifswald.de
(Received 9 April 2004; first review notified 21 May 2004; in revised form 11 June 2004; accepted 12 June 2004)
Aims: To examine the immune consequences of chronic alcoholism in man, in relation to the known association between alcoholism and raised incidence and severity of infections. Methods: In 36 alcoholics without liver disease, at the point of commencing withdrawal from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin-neutralizing capacity (ENC) of the serum, titers of anti-lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNF
, IL1ß, IL1RA, IL4, IL6, IL8, IL10 and IL12). The results were compared to those from healthy volunteers (day controls). Measures were repeated after 8–13 days of abstinence. Results: LPS-binding protein (LBP) and soluble CD14 (sCD14) were significantly increased in patients' sera at the outset of withdrawal, whereas reduced titers of anti-LPS IgG (P = 0.012) and a reduced ENC (P = 0.001) were measured. Only ENC rapidly returned to normal values after withdrawal therapy. Cytokine induction with phorbol ester showed no significant alterations in patients' T cells. Patients' monocytes, however, responded to LPS stimulation with enhanced IL1ß-, but reduced TNF- and IL12-production (P = 0.004, P = 0.0042 and P = 0.001, respectively). While IL1- and TNF-responses normalized after the withdrawal period, impairment of the IL12 response persisted throughout the observation period of 2 weeks. Conclusions: Alcoholism results in a prolonged LPS-mediated hypoinflammatory conditioning of the innate but not the adaptive immune system, which is not reversed immediately after withdrawal. This alcohol-induced status of the immune system predisposes to infections and sepsis by blunting initial response to the pathogens.
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