Regulatory Potential of Ethanol and Retinoic Acid on Human Monocyte Functions

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Abstract
Retinoic acid (RA), a metabolic product of vitamin A, has been shown to affect a variety of immune functions, including monocytes. Monocyte functions and mediator production are also modulated by ethanol exposure. This study demonstrates that therapeutic doses of RA (0.1–10 μM) significantly increase transforming growth factor‐β (TGFβ) production both in THP‐1, human myelomonocytic cells, and in human peripheral blood monocytes. We have previously reported TGFB induction by ethanol in human Mø. Combination of RA stimulation with acute in vitro ethanol treatment, however, resulted in significantly lower Mø TGFβ production than TGFB levels induced by RA alone (p < 0.003). Down‐regulation of Mø TGFβ production by ethanol was tested at the concentration range of 25–150 mM and occurred both at high and low RA concentrations (10–0.1μM). In contrast to its inhibitory effect on RA‐induced Mø TGFβ production, ethanol augmented TGFB production induced by mura‐my1 dipeptide (20 μg/ml), suggesting that ethanol can either up‐ or down‐regulate Mø TGFB production, depending on the costimulatory factors. RA also induced a moderate increase in Mø tumor necrosis factor‐α (TNFα) production, which was down‐regulated by ethanol both at the level of secreted and cell‐associated TNFα. In addition to regulation of cytokine production, both RA and ethanol decreased expression of CD4 on THP‐1 cells. The degree of inhibition of CD4 expression by RA was more significant than by ethanol, but RA‐induced decrease in CD4 expression was not significantly affected by the combined stimulation with ethanol. These results provide further evidence for the immunoregulatory potential of nutritional and dietary factors, such as RA and ethanol, on the immune functions of human monocytes.

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