Down-regulation of tumor necrosis factor alpha activity by acute ethanol treatment in human peripheral blood monocytes

UMMS Affiliation

Department of Surgery; Department of Medicine, Division of Gastroenterology

Publication Date


Document Type



Acetylmuramyl-Alanyl-Isoglutamine; Adult; Aged; Cell Adhesion; Cell Separation; Cell Survival; Dinoprostone; Dose-Response Relationship, Drug; Down-Regulation; Ethanol; Female; Flow Cytometry; Humans; Indomethacin; Interferon-gamma; Macrophage Activation; Male; Middle Aged; Monocytes; Receptors, IgG; Tumor Necrosis Factor-alpha


Digestive System Diseases | Gastroenterology


As the most commonly used drug that can modulate both metabolic and immune pathways, ethanol is evaluated in this report as a regulator of tumor necrosis factor alpha (TNF alpha) production in human peripheral blood monocytes (M phi) in combination with a variety of stimuli. While acute ethanol treatment did not induce TNF alpha in M phi, it was a potent down-regulator of M phi TNF alpha production whether induced by the combination of interferon-gamma plus muramyl dipeptide (MDP) (P < 0.001), lipopolysaccharide (LPS) alone (P < 0.01), or interferon-gamma plus LPS. Down-regulation of M phi TNF alpha by ethanol was dose dependent and statistically significant in the biologically relevant, 25-150 mM, ethanol concentration range. We also demonstrate that these ethanol concentrations did not affect M phi viability. TNF alpha down-regulation by ethanol was most effective when ethanol was administered 4 hr prior to MDP stimulation; however, it was also effective--though to a lesser extent--if it was added at the time of MDP stimulation. Furthermore, ethanol also down-regulated TNF alpha production of the in vivo preactivated M phi of trauma patients, which produce hyperelevated levels of TNF alpha. We have previously shown that the majority of posttrauma elevated M phi TNF alpha is produced by the M phi subpopulation expressing high-affinity type I Fc gamma receptors (Fc gamma RI). When the Fc gamma RI cross-linking-stimulated M phi subpopulation was treated with acute ethanol, TNF alpha production was suppressed again both in in vivo preactivated M phi of trauma patients and in M phi of normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)


J Clin Immunol. 1993 Jan;13(1):8-22.

Journal/Book/Conference Title

Journal of clinical immunology

Related Resources

Link to Article in PubMed

PubMed ID