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Background  Excessive alcohol intake is associated with adverse immune response-related effects, however, acute and chronic abuse differently modulate monocyte activation. In this study, we have evaluated the phenotypic and functional changes of monocytes in acutely intoxicated healthy volunteers (HV).    Methods  Twenty-two HV consumed individually adjusted amounts of alcoholic beverages until reaching a blood alcohol level of 1‰ after 4h (T4). Peripheral blood was withdrawn before and 2h (T2), 4h (T4), 6h (T6), 24h (T24), and 48h (T48) after starting the experiment and stained for CD14, CD16 and TLR4. CD14 bright CD16 - , CD14 bright CD16 +  and CD14 dim CD16 +  monocyte subsets and their TLR4 expression were analyzed by flow cytometry. Inflammasome activation  via  caspase-1 in CD14 +  monocytes was measured upon an  ex vivo in vitro  LPS stimulation. Systemic IL-1β and adhesion capacity of isolated CD14 +  monocytes upon LPS stimulation were evaluated.    Results  The percentage of CD14 +  monocyte did not change following alcohol intoxication, whereas CD14 bright CD16 -  monocyte subset significantly increased at T2 and T24, CD14 bright CD16 +  at T2, T4 and T6 and CD14 dim CD16 +  at T4 and T6. The relative fraction of TLR4 expressing CD14 +  monocytes as well as the density of TLR4 surface presentation increased at T2 and decreased at T48 significantly. TLR4 + CD14 +  monocytes were significantly enhanced in all subsets at T2. TLR4 expression significantly decreased in CD14 bright CD16 -  at T48, in CD14 bright CD16 +  at T24 and T48, increased in CD14 dim CD16 +  at T2. IL-1β release upon LPS stimulation decreased at T48, correlating with TLR4 receptor expression. Alcohol downregulated inflammasome activation following  ex vivo in vitro  stimulation with LPS between T2 and T48  vs . T0. The adhesion capacity of CD14 +  monocytes decreased from T2 with significance at T4, T6 and T48. Following LPS administration, a significant reduction of adhesion was observed at T4 and T6.    Conclusions  Alcohol intoxication immediately redistributes monocyte subsets toward the pro-inflammatory phenotype with their subsequent differentiation into the anti-inflammatory phenotype. This is paralleled by a significant functional depression, suggesting an alcohol-induced time-dependent hyporesponsiveness of monocytes to pathogenic triggers.

Acute Alcohol Intoxication Modulates Monocyte Subsets and Their Functions in a Time-Dependent Manner in Healthy Volunteers