They gave the participants four to five shots of vodka—enough to qualify as binge drinking. The researchers took blood samples from the participants three times after they reached peak intoxication. Twenty minutes after hitting their booze high, the participants’ immune systems were actually stronger than normal. They had higher counts of three white blood cells and more cytokines, special proteins that accompany immune activity.
The association between genetically predicted levels of alcohol consumption and risk of common autoimmune inflammatory diseases. Although most research has focused on the effects of heavy alcohol consumption on the immune system, several studies have also confirmed that even moderate consumption can have significant effects on the immune system. For example, one study found that women who consumed 330 mL of beer for 30 days exhibited a significant increase in leukocytes, mature CD3+ T-cells, neutrophils, and basophils.
In addition, Jα18-/- mice (a knockout model deficient in iNKT cells) demonstrated significantly higher levels of total NK-cell count and IFN-γ release following alcohol exposure, while WT Twelve-step program mice exhibited a loss of total NK cells and IFN-γ. Likewise, iNKT-deficient Jα18-/- mice appeared relatively protected from hepatic steatosis, but if these mice were also depleted of their NK cells by using the anti-AsGM1 antibody, alcoholic liver injury steatosis was significantly aggravated. Further, hepatic IL-10 was significantly upregulated, but no changes in TGF-β or IL-4 were noted.
These micronutrients have been shown to play an important role in immune system homeostasis and response to infection (Mora, Iwata et al. 2008). Past research shows alcohol consumption leads to more severe lung diseases, like adult respiratory distress syndrome (ARDS) and other pulmonary diseases, including pneumonia, tuberculosis, and respiratory syncytial virus. The white blood cells had cleared out, and a new type of cytokines—ones that signal a decrease in immune activity—had appeared in the participants’ blood.
Additional studies are required to fully understand the role of ethanol metabolites and adducts in the development of alcoholic liver injury and organ damage. Though there’s still limited data on the link between alcohol and COVID-19, past evidence shows alcohol consumption can worsen the outcomes from other respiratory illnesses by damaging the lungs and gut, and impairing the cells responsible for immune function. NIAAA also includes a category for binge drinking — drinking a very large amount of alcohol in a short amount of time. While the actual definition is based on https://ecosoberhouse.com/ an individual’s change in blood alcohol levels, the NIAAA states that, in an average adult, drinking four or more drinks for women or five or more for men in two hours will typically be considered binge drinking. Factors such as the amount of alcohol a person drinks, how often a person drinks, the type of alcohol they drink, and whether they are biologically male or female can increase or decrease how much it affects their immune system.
Here, alcohol can damage the epithelial cells, T-cells, and neutrophils in the GI tract, all of which can alter the gut barrier function and allow intestinal microorganisms to leak into circulation. The adaptive immune system can be further subdivided into cell-mediated immunity and humoral immunity. Whereas T-cells are primarily involved with cell-mediated immunity, B-cells play a major role in humoral immunity. Alcoholic beverages are energy dense and often become the primary energy source in those with AUD, leading to malnutrition. Individuals with AUD does alcohol suppress immune system are often deficient in one or more essential nutrients including vitamin A, vitamin C, vitamin D, vitamin E, folate, and thiamine (Hoyumpa 1986).
DCs uptake antigens in peripheral tissues which leads to their maturation, and then travel to draining lymph nodes where they present them to T cells (Janeway 2008). Similarly, consumption of 10% (w/v) ethanol in tap water ad libitum for 2 days in mice resulted in decreased bone marrow DC generation, decreased expression of CD80 and CD86, impaired induction of T cell proliferation, and a decrease in IL-12 production (Lau, Abe et al. 2006). Alcohol-fed animals showed that reduced T cell proliferation and altered CD4 and CD8 T cell counts were major reasons for pulmonary tuberculosis in infected animals 60. Animal studies reported that alcohol intoxication leads to suppressed pro-inflammatory cytokines, such as IL-12 and interferon‐gamma (IFN‐γ); however, this pro-inflammatory suppression due to alcohol mediated the increase in anti-inflammatory cytokine IL-10 61,62.