BACKGROUND: Alcohol affects both innate and acquired immune responses. Chronic alcoholics have reduced delayed-type hypersensitivity response and increased susceptibility to infections. In contrast, recent studies suggest that acute, moderate alcohol consumption has protective effects on mortality. Monocytes and dendritic cells (DC) play a central role in coordination of innate and adaptive immune responses and are pivotal in activation of T lymphocytes in an antigen-specific manner. In this study, we investigated the effects of acute, moderate alcohol consumption on antigen presenting cell function of blood monocytes and monocyte-derived myeloid dendritic cells. METHODS: Accessory cell function of human blood monocytes was tested before and after acute alcohol intake (2 ml vodka/kg body weight) by measuring T cell activation with alloantigen (mixed lymphocyte reaction, MLR), superantigen (staphylococcal enterotoxin B) and recall antigen (tetanus toxoid). Myeloid DCs were generated in vitro from monocytes obtained from these individuals using IL-4 and GM-CSF and their allostimulatory function was tested in an MLR. RESULTS: We found significantly reduced T cell proliferation in the presence of monocytes obtained 2 or 18 hr after alcohol consumption whether alloantigen, superantigen, or recall antigen was the stimuli (p < 0.01). The reduced T cell proliferation was due to the effects of acute alcohol on monocytes rather than on T cells as we found decreased proliferation only in the presence of alcohol-exposed accessory cells but not when T cells were exposed to alcohol. In addition, monocyte-derived dendritic cells showed significantly reduced allostimulatory capacity after alcohol consumption (p < 0.005). CONCLUSION: Acute alcohol consumption inhibits accessory cell function of both monocytes and myeloid dendritic cells. Impaired function of these key antigen-presenting cells may contribute to reduced adaptive immune responses and increased susceptibility to infections when acute alcohol intake coincides with exposure to pathogens.
BACKGROUND:Alcohol affects both innate and acquired immune responses. Chronic alcoholics have reduced delayed-type hypersensitivity response and increased susceptibility to infections. In contrast, recent studies suggest that acute, moderate alcohol consumption has protective effects on mortality. Monocytes and dendritic cells (DC) play a central role in coordination of innate and adaptive immune responses and are pivotal in activation of T lymphocytes in an antigen-specific manner. In this study, we investigated the effects of acute, moderate alcohol consumption on antigen presenting cell function of blood monocytes and monocyte-derived myeloid dendritic cells. METHODS: Accessory cell function of human blood monocytes was tested before and after acute alcohol intake (2 ml vodka/kg body weight) by measuring T cell activation with alloantigen (mixed lymphocyte reaction, MLR), superantigen (staphylococcal enterotoxin B) and recall antigen (tetanus toxoid). Myeloid DCs were generated in vitro from monocytes obtained from these individuals using IL-4 and GM-CSF and their allostimulatory function was tested in an MLR. RESULTS: We found significantly reduced T cell proliferation in the presence of monocytes obtained 2 or 18 hr after alcohol consumption whether alloantigen, superantigen, or recall antigen was the stimuli (p < 0.01). The reduced T cell proliferation was due to the effects of acute alcohol on monocytes rather than on T cells as we found decreased proliferation only in the presence of alcohol-exposed accessory cells but not when T cells were exposed to alcohol. In addition, monocyte-derived dendritic cells showed significantly reduced allostimulatory capacity after alcohol consumption (p < 0.005). CONCLUSION: Acute alcohol consumption inhibits accessory cell function of both monocytes and myeloid dendritic cells. Impaired function of these key antigen-presenting cells may contribute to reduced adaptive immune responses and increased susceptibility to infections when acute alcohol intake coincides with exposure to pathogens.
Authors: Ji Fan; Michelle R Edsen-Moore; Lucas E Turner; Robert T Cook; Kevin L Legge; Thomas J Waldschmidt; Annette J Schlueter Journal: Alcohol Clin Exp Res Date: 2010-10-06 Impact factor: 3.455
Authors: Elizabeth Porretta; Kyle I Happel; Xu S Teng; Alistair Ramsay; Carol M Mason Journal: Alcohol Clin Exp Res Date: 2011-10-20 Impact factor: 3.455
Authors: Samikkannu Thangavel; Carmen T Mulet; Venkata S R Atluri; Marisela Agudelo; Rhonda Rosenberg; Jessy G Devieux; Madhavan P N Nair Journal: Antioxid Redox Signal Date: 2018-02-01 Impact factor: 8.401