Alcohol and Your Immune System: Does It Help or Hurt?

Studies over the last 30 years have clearly demonstrated that chronic ethanol abuse impairs the functions of both T cells and B cells. Chronic alcohol consumption results in lymphopenia with a loss in circulating T cells and B cells. The decrease in T cells is does alcohol compromise your immune system accompanied by increased homeostatic proliferation, which in turn leads to increased T-cell differentiation, activation, and conversion to the memory phenotype. Impairment in T-cell recruitment also was observed in mouse models of chronic alcohol exposure.

Finally, chronic alcohol exposure in utero interferes with normal T-cell and B-cell development, which may increase the risk of infections during both childhood and adulthood. Alcohol’s impact on T cells and B cells increases the risk of infections (e.g., pneumonia, HIV infection, hepatitis C virus infection, and tuberculosis), impairs responses to vaccinations against such infections, exacerbates cancer risk, and interferes with delayed-type hypersensitivity. In contrast to these deleterious effects of heavy alcohol exposure, moderate alcohol consumption may have beneficial effects on the adaptive immune system, including improved responses to vaccination and infection. The molecular mechanisms underlying ethanol’s impact on the adaptive immune system remain poorly understood.

Cancer risk

These clinical observations were confirmed with cultured cells as well as in rodent studies. Treatment of a mouse cell line (i.e., A78-G/A7 hybridoma cells) with different concentrations of ethanol (25, 50, 100, and 200mM) for 48 hours resulted in a linear increase in IgM levels (Muhlbauer et al. 2001). Moreover, spontaneous IgA synthesis by peripheral blood mononuclear cells (PBMCs)— a mixed population of various white blood cells that also includes B cells—was higher in PBMCs isolated from alcoholic patients with liver disease compared with controls (Wands et al. 1981). IgA concentrations also were increased in a layer (i.e., the lamina propria) of the mucous membranes lining the intestine of adult female Wistar rats after acute ethanol administration (4g/kg intraperitoneally) for 30 minutes (Budec et al. 2007).

While antibiotics do not prevent the induction of TLR mRNA production, inhibition of the nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) is effective in limiting hepatic TNFα levels [29]. These data indicate that reactive oxygen species (ROS) play an important role in inflammation, which is induced by chronic alcohol consumption [29]. Nevertheless, TLR3 examined in a binge-drinking mouse model with TLR3-/- and IL-10-/- knockout mice seemed to have an antagonistic effect to TLR4. Treatment with polyinosinic-polycytidylic acid, a TLR3 ligand, decreases TNFα, IL-6, MCP-1, and FAS gene expression, and enhances IL-10 gene expression in the qRT-PCR analysis in isolated Kupffer cells as well as in hepatic stellate cells [30].

The Adaptive Immune Response

Alcohol metabolism can also take place in the pancreas by acinar and pancreatic stellate cells, which contributes to the development of alcoholic pancreatitis (Vonlaufen, Wilson et al. 2007). Additional studies are required to fully understand the role of ethanol metabolites and adducts in the development of alcoholic liver injury and organ damage. The constant low-level inflammation from the aging innate immune system can damage tissues throughout the body, increasing the risk of heart disease, Alzheimer’s, Parkinson’s, osteoarthritis and many other diseases. During adulthood, the T and B cells in the adaptive immune system decline in number and function, making it more challenging for the body to fight infections. Alcohol alters the composition of the IMB, resulting in an alteration of the amount and type of neuroactive substances produced by the microbiota, which may lead to behavioral alteration [79]. Gut–brain communication is disrupted by alcohol-related immune and gut dysfunction [80].