How Alcohol Can Affect Your Immune System

Drinking also makes it harder for your body to properly tend to its other critical functions, like fighting off a disease. “With COVID-19, alcohol is likely to interfere with an individual’s ability to clear SARS-CoV-2 and cause people to suffer worse outcomes, including ARDS, which commonly results in death,” Edelman said. When the body is unable to clear a pathogen, an infection can worsen and lead to more severe, life threatening complications.

These findings suggest that ethanol pretreatment can sensitize T cells to AICD (Kapasi et al. 2003). In vivo studies in humans confirmed these observations, demonstrating that binge drinking (i.e., consuming 5 to 7 drinks within 90 to 120 minutes) promoted T-cell apoptosis and decreased Bcl-2 expression (Kapasi et al. 2003). Summarizing this, it is evident that alcohol significantly impacts different cells of the innate immune arm, and different tissues, by modulating phagocytosis and/or oxidative burst. Mostly chronic alcohol consumption goes hand in hand with impaired macrophage and/or neutrophil functions. In conclusion, alcohol can enable pathogens to enter the systemic blood flow, a process that may lead to an increased susceptibility of patients with infections. Furthermore, the induction of DAMPs in a sterile environment by alcohol should be a focus of further research, because, potentially, this may provide novel understanding of the chronic inflammation after alcohol consumption in case of no visible damage to organs.

The Gastrointestinal Microbiome: Alcohol Effects on the Composition of Intestinal Microbiota

Also, being obese seems to make you more likely to get the flu and other infections, like pneumonia. Alcohol’s effects on the structural host defense of the gastrointestinal (GI) tract. Alcohol-induced changes in tight junctions cause increased intestinal leaks that lead to translocation of bacteria-derived products such as lipopolysaccharide (LPS).

This reduced class I MHC expression can result from infection with certain types of viruses. The cell-mediated arm of the innate immunity is orchestrated primarily by granulocytes, monocytes/macrophages, dendritic does alcohol compromise your immune system cells, and natural killer (NK) cells. Granulocytes are white blood cells (i.e., leukocytes) that derive their name from the large granules that are visible when the cells are stained for microscopic analysis.

How does alcohol affect your immune system?

In addition, alcohol markedly affects the differentiation of dendritic cells in blood and tissues (Ness et al. 2008). The alcohol-induced defects in dendritic cell function include reduced levels of CD80 and CD86 on the cells’ surface (which are necessary to induce activation of T-cells) as well as reduced production of IL-12, which is critical for stimulating naïve CD4+ T-cells to become IFN-γ–producing Th1 cells. The induced innate humoral response plays a critical role in clearing or containing infection while an adaptive response develops. It is characterized by the release of mediators of inflammatory reactions, such as cytokines and chemokines, as well as activation of the complement cascade.

• Although NF-κB signaling is detrimental in the alcohol-induced innate immune response, there is still a knowledge gap on the level of its target genes, caused probably by the individual variations of NF-κB activation.
• Furthermore, ethanol exposure decreased expression of the anti-apoptotic molecule Bcl-2 and promoted expression of the pro-apoptotic molecule BAX in the cells.
• It constitutes the first line of defense against molecules, which are either pathogen-derived or a danger signal themselves, and not seldom both.
• Nevertheless, studies have shown that the normal gut microbiota comprises mainly Bacteroidetes and Firmicutes as the dominant phyla, followed by Actinobacteria and Verrucomicrobia.
• Specifically, 24 hours of exposure to both low (1mM) and high (5mM) concentrations of acetaldehyde stimulate IL-6 secretion, however, 7 days of exposure to the high concentration of acetaldehyde, significantly decrease IL-6 secretion (Sarc, Wraber et al. 2011).

The induction of canonical NF-κB with p50–p65 translocation to nucleus via pattern recognition receptors (PRR) is outlined by, for example, TLR4 and MyD88 activation. The non-canonical NF-κB pathway with p52-RelB is detailed with CD40 as the respective receptor. Another cell compartment under alcohol influence is the phagosome needed for ingestion and destruction of pathogens using an array of reactive oxygen species. Few studies have investigated the effects of alcohol abuse on complement activation and its relationship with the incidence and severity of infection; instead, the focus of studies on alcohol-induced alterations in complement has been on liver injury (Pritchard et al. 2008). However, alcoholic patients frequently have abnormally low levels of complement in the blood. In addition, animal studies have indicated that acute alcohol intoxication can decrease complement activation in response to tissue injury resulting from disruptions in blood supply (i.e., ischemic injury).