Excessive alcohol consumption is known to worsen the effects of disease, resulting in longer recovery period after trauma, injury or burns. It is also known to impair the anti-viral immune response, especially in the liver, including response against Hepatitis C (HCV) and HIV. New research suggests that alcohol modulates the anti-viral and inflammatory functions of monocytes and that prolonged alcohol consumption has a double negative effect of reducing the anti-viral effect of Type 1 interferon (IFN) whilst increasing inflammation via the pro-inflammatory cytokine TNF± .
Source: Inhibition of TLR8- and TLR4-induced Type I IFN induction by alcohol is different from its effects on inflammatory cytokine production in monocytes.Maoyin Pang , Shashi Bala , Karen Kodys , Donna Catalano and Gyongyi Szabo.BMC Immunology 2011, 12:55doi:10.1186/1471-2172-12-55
Gyongyi Szabo, MD, PhD, Associate Dean of clinical and translational sciences, professor of gastroenterology at the University of Massachusetts Medical School and colleagues examined the effect of alcohol on monocytes collected from the blood of healthy volunteers. The study focussed specifically on two disease related pathways - the first (Toll-like receptor 8 - TLR8) stimulated by single strand RNA viral attack and the second (TLR4) is involved in recognising bacteria.
Their results suggest that activation of these pathways resulted in an increase in the levels of the anti-viral cytokine IFN. However, this was reduced by treatment with alcohol equivalent to four or five drinks a day for seven days. Similarly, stimulation of these pathways resulted in an increase in the levels of the pro-inflammatory cytokine TNF±. While a single treatment with alcohol decreased the amount of TNF±, prolonged treatment increased levels of inflammation.
Dr Szabo said “Alcohol has a profound effect of inhibiting IFN production in monocytes regardless of whether the danger signal is intracellular (TLR8) or surface-derived (TLR4). Such a reduction would impair the body’s ability to fight off infection. Additionally, the fact that Type I IFN production is depressed despite increased levels of the pro-inflammatory cytokine TNF±, due to chronic alcohol exposure suggests that prolonged alcohol misuse must change the immune balance of monocyte activation and impair host response to single-stranded virus infection like hepatitis C”.