Moderate Alcohol Intake in Humans Attenuates Monocyte Inflammatory Responses: Inhibition of Nuclear Regulatory Factor Kappa B and Induction of Interleukin 10

Abstract

Our findings suggest that acute alcohol consumption has dual anti-inflammatory effects that involve augmentation of IL-10 and attenuation of monocyte inflammatory responses involving inhibition of NF-kappaB. These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis.

Production of inflammatory cytokines by peripheral blood monocytes in chronic alcoholism: Relationship with ethanol intake and liver disease

“…In line with this, it has been reported that acute in vitro exposure to ethanol (EtOH) decreases production of inflammatory cytokines (i.e., interleukin [IL] 1, IL6, and tumor necrosis factor a [TNFa]) by human monocytes (4)(5)(6)(7)(8) and macrophages (i.e. TNFa) (9), these effects being mediated through toll-like receptors (TLR) (10).…”

In vitroandin vivomodels of acute alcohol exposure

“…In vivo the consumption of alcohol in one setting implies that the entire dose of alcohol is consumed at once, while a 'binge' is defined by NIAAA as an excessive pattern of alcohol drinking that produces BAL greater than 0.08% within a 2-h period and may, or may not, be associated with dependence [11,12,17,18] . Thus any model using consumption of biologically active amounts of alcohol within 2 h is considered an acceptable model of AAA [81,[107][108][109][110][111][112][113][114][115][116][117][118][119][120][121] . (2) Establish an exposure to an accurate concentration of ethanol.…”

“…For in vitro studies the 10-100 mmol/L ethanol range is considered physiological, with 25 mmol/L ethanol being close to 0.08% BAL achieved in vivo after 4-5 drink equivalents [7,11,12,[98][99][100][101][102][103][104][105][106] . For the in vivo studies an 0.08% BAL or above this level yields signs of intoxication and it is employed in the majority of biomedical studies [107][108][109][110][111][112][113][114][115][116][117][118][119][120][121] . (3) Recruit individuals who are currently not and never have been alcohol abusers for in vivo studies and employ alcohol-naïve primary cells or cell lines for in vitro studies.…”

Alcohol Effects on TNF-α and IL-10 Production in an Ex-Vivo Model of Whole Blood Stimulated by LPS

“…In contrast, although the combined stimulation of 25 mM ethylic alcohol and LPS did not significantly changed IL-10 production after 10 h stimulation, 100mM alcohol and LPS significantly decreased monocyte IL-10 production than LPS alone [36]. Several other studies using a completely different protocol including drinking of alcohol in healthy volunteers and blood receipt after 18-24 hours, which was stimulated with or without LPS, found a significant increase in IL-10 production [37][38][39][40]. These findings do not contrast our results since a shorter timeframe was applied in our experiments in addition to the use of whole blood in an ex-vivo environment.…”

“…Acute alcohol exposure in vivo and in vitro induced IL-10 production in human monocytes, with or without LPS stimulation [32,[36][37][38][39][40]41], and thus may interfere with the cell-mediated and humoral immunity by both reducing inflammatory cytokine production and preventing T-cell proliferation [17,36,42].…”