Ethanol-Induced Suppression of in Vivo Host Defense Mechanisms to Bacterial Infection

Abstract

Study findings have shown that chronic ethanol (ETOH) abuse causes individuals to have an increased incidence of infections related to opportunistic and pathogenic organisms (1–3). This is particularly true for bacterial pneumonias, which cause greater mortality in alcoholics as compared with nonalcoholics. Alcoholics also have an increased incidence of tumors of the head, neck, and gastrointestinal tract (4,5). Individuals with alcohol-induced liver cirrhosis have circulating lymphocytes that are cytotoxic to hepatocytes, suggesting that ETOH may induce an immune dysfunction that leads to autoimmunity (6-8). Although the exact role of ETOH in these diseases is not well understood, its effects on both specific and nonspecific aspects of immune function are thought to be involved. With ETOH consumption, many of the nonspecific aspects of immune function are altered. For example, consumption of ETOH by mice leads to depressed natural killer cell activity (9). Ethanol consumption also results in diminished granulocyte function such as decreased phagocytosis and altered migration to chemotactic factors by polymorphonuclear leukocytes (10,11). Ethanol directly alters monocyte and macrophage functions in human beings and experimental animals. For example, exposure of human macrophages to ETOH in vitro reduces the production and release of lysozyme, as well as the total number of macrophages containing lysozyme (12). Furthermore, study findings have shown that ETOH impairs phagocytosis in human monocytes and macrophages (13). Similar results have been obtained by investigators examining the effects of ETOH on rat peritoneal, alveolar, and splenic macrophages (14,15).