Abstract
Background: Epidemiological data indicate that among alcoholics African-American men have higher rates of infections compared with white alcoholics. Alcohol is thought to reduce natural killer (NK) cell responses and to alter cellular immunity by changing the relative balance of Th1 versus Th2 cytokine response profiles. However, translation of these basic immunological observations into the clinical setting is limited, and what clinical data are available are contradictory, in part, because of heterogeneity within the alcoholic patient population. Whether ethnic characteristics contribute to variation in the immunological effects of alcohol is not known. Methods: This study compared NK activity, interleukin (IL)-2–stimulated NK activity, and concanavalin A–stimulated peripheral blood mononuclear cell production of Th1 (IL-12 and IL-2), Th2 (IL-10), and proinflammatory (IL-6) cytokines in 31 hospitalized chronic alcoholic patients and 31 age-matched controls who were stratified on the basis of ethnicity. Results: NK-cell responses were significantly different across the four groups, and African-American alcoholics showed the lowest levels of NK activity (F= 9.5;p < 0.001) and IL-2–stimulated NK activity (F= 2.9;p < 0.05). Compared with the other three groups, African-American alcoholics also showed lower levels of IL-6 (F= 7.2;p < 0.01) and higher levels of IL-10 (F= 4.9;p < 0.05). Stimulated production of IL-2 and IL-12 were similar in the four groups. Regression analyses showed that alcohol dependence and ethnicity predicted NK activity, whereas the interaction between alcohol dependence and ethnicity predicted levels of IL-6 and IL-10. Conclusions: In summary, the immunological effects of alcohol dependence are modified by ethnicity status, consistent with the increased health risks found in African-American alcoholics.
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