ETHANOL AUGMENTS INTRACELLULAR SURVIVAL OF MYCOBACTERIUM-AVIUM COMPLEX AND IMPAIRS MACROPHAGE RESPONSES TO CYTOKINES
ETHANOL AUGMENTS INTRACELLULAR SURVIVAL OF MYCOBACTERIUM-AVIUM COMPLEX AND IMPAIRS MACROPHAGE RESPONSES TO CYTOKINES
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DOI:
10.1093/infdis/163.6.1286
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发表时间:
1991-06-01
影响因子:
6.4
通讯作者:
YOUNG, LS
中科院分区:
文献类型:
--
作者:
BERMUDEZ, LE;YOUNG, LS
Chronic ethanol ingestion predisposes to tuberculosis and bacterial pneumonia. Mycobacterium avium complex (MAC) organisms cause bacteremia in patients with AIDS. Cultured human monocyte-derived macrophages and murine Kupffer cells were exposed to 10-100-mu-g/dl ethanol; significantly greater intracellular growth of MAC strains 100 (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-mu-g/dl ethanol vs. control). Both cell types, when treated with 10(3) units/ml recombinant tumor necrosis factor (TNF) or 10(2) units/ml granulocyte-macrophage colony-stimulating factor (GM-CSF) in the presence of 10-100-mu-g/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 the host and MAC favor progressive infection.