Ethanol Augments Intracellular Survival of Mycobacterium avium Complex and Impairs Macrophage Responses to Cytokines

Abstract
Chronic ethanol ingestion predisposes to tuberculosis and bacterial pneumonia. Mycobacterium avium complex (MAC) organisms cause bacteremia in patients withAIDS. Cultured human-monocyte-derived macrophages and murine Kupffer cells were exposed to 10–100 µg/dl ethanol; significantly greater intracellular growth of MAC strains1 00 (serovar 8) and 101 (serovar 1)occurred in ethanol-treated cells than in controls (range, 58% ± 7%–70% ± 5%; P < .05 for 50 and 100 µg/dl ethanol vs. control). Both cell types, when treated with 103 units/ml recombinant tumor necrosis factor (TNF) or 102 units/ml granulocyte-macrophage colony-stimulating factor (GM-CSF) in the presence of 10–100 I-tg/dl ethanol,killed significantly fewer MAC than controls (49% ± 12% decrease for GM-CSF and 57% ± 16% for TNF; P < .05 for all comparisons). C57BL black mice infected intravenously with MAC strain 101 were given ethanol as 4% of total calories daily; after 21 days they had greater numbers of MAC in blood, liver, and spleen than controls. Ethanol's effects on the interaction between theh ost and MAC favor progressive infection.