Alcohol impairs the body’s ability to fight off viral infection
Alcohol 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 published in BioMed Central’s open access journal BMC Immunology shows 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 TNFα.
Researchers from the University of Massachusetts Medical School looked at the effect of alcohol on monocytes collected from the blood of healthy volunteers. The group, led by Prof Gyongyi Szabo, 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 showed that, as expected, 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 TNFα. However, while a single treatment with alcohol decreased the amount of TNFα, prolonged treatment increased levels of inflammation.
Prof 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, TNFα, due to chronic alcohol exposure suggests that prolonged alcohol must change the immune balance of monocyte activation and impair host response to single-stranded virus infection like hepatitis C.”
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Notes to Editors
1. 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 (in press)
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Alcohol abuse and hepatitis C virus (HCV) infection coexist with chronic liver disease in many patients. The mechanism of injury in these patients is probably multifactorial and involves, but is not limited to, a combination of diminished immune clearance of HCV, oxidative stress, emergence of HCV quasi-species, hepatic steatosis, increased iron stores, and increased rate of hepatocyte apoptosis. In patients with HCV infection, alcohol consumption is known to cause accelerated progression of liver fibrosis, higher frequency of cirrhosis, and increased incidence of hepatocellular carcinoma (HCC). These patients also have decreased survival as compared with patients with either alcohol abuse or HCV liver injury alone. Alcohol abuse causes decreased response to interferon treatment in HCV patients. It is therefore necessary for patients with HCV infection to abstain from alcohol consumption.
Introduction
Chronic hepatitis C infection and alcohol abuse account for 70 to 90% of all the cases of chronic liver diseases in the western world. About 20% of chronic alcoholics and patients with hepatitis C infection develop cirrhosis over a period of 20 to 30 years and a portion of these patients develop HCC. Hepatitis C-related cirrhosis now accounts for more than 50% of all liver transplants performed in the United States.
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Kamran Safdar, M.D.; Eugene R. Schiff, M.D.
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Dr Hilary Glover
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44-020-319-22370
BioMed Central