Moderate alcohol consumption and the immune system: a review

Increases in IL-7 and IL-15, which are critical for T cell survival, may be compensatory mechanisms for reduced IL-2 levels. Reduced IgE levels were also observed and may be related to the observed decrease in IgE synthesis regulators, IL-13 and CD40 ligand. Increased levels of CCL11, a potent chemokine for IgE-producing eosinophils, may be compensating the reduced IgE levels (Helms, Messaoudi et al. 2012). Beyond that, long-term alcohol use leads to the breakdown of the liver or liver failure. Alcohol may also affect an addicted individual’s ability to store adequate amounts of protein. Overall, prolonged alcoholism may result in autoimmunity, a phase of the immune system during which the body attacks its own tissues.

“Alcohol has diverse adverse effects throughout the body, including on all cells of the immune system, that lead to increased risk of serious infections,” said Dr. E. Jennifer Edelman, a Yale Medicine addiction medicine specialist. These observations suggest that immune defects seen in individuals with AUD could also be mediated by nutritional deficiencies in addition to barrier defects and functional changes in immune cells. However, the contributions of each of these changes does alcohol compromise your immune system to increased susceptibility to infection in individuals with AUD remain to be determined. That’s because your body can’t make as many infection-fighting cells and proteins called antibodies that help defend against illness. Your body releases certain proteins that help the immune system, called cytokines, only during sleep. As described earlier for adult humans, alcohol can lead to increases in Ig levels during development, even if the numbers of mature B cells decrease.

Short-term effects of alcohol on the immune system

Indeed, in utero exposure to ethanol resulted in a significant reduction in T-cell and B-cell responses to various antigens that did not recover to control levels until 4 to 5 weeks of life. In contrast, ethanol exposure did not significantly affect the development of the lytic functions of NK cells (Wolcott et al. 1995). Activated T cells normally undergo apoptosis if they receive a second activation stimulus within a short interval. This process is known as activation-induced cell death (AICD) and is important to maintain T-cell homeostasis and self-tolerance (Alderson et al. 1995). Experiments done in an immortalized line of human T lymphocyte cells used in cancer research (i.e., Jurkat cells) found that exposure to different concentrations of ethanol (i.e., 25, 50, 100, 150, 200 mM) for 24 hours resulted in decreased cell viability in a dose-dependent manner. Furthermore, ethanol exposure decreased expression of the anti-apoptotic molecule Bcl-2 and promoted expression of the pro-apoptotic molecule BAX in the cells.

Their main role is to capture, ingest, and process antigens in order to present them on their surface to cells of the adaptive immune response (i.e., to the T-lymphocytes). Thus, dendritic cells play a crucial role in linking innate and adaptive immune responses. Lastly, NK cells are abundant in the liver (Gao et al. 2009) and recognize cells that have low levels of a protein called class I major histocompatibility complex (MHC) on their surface.

Effects of Alcohol on Immune System: Putting All the Pieces Together

In an unstimulated milieu, the above mentioned p100 processing is inhibited by degradation of NF-κB-inducing kinase (NIK) [43]. Here, TRAF3 rapidly binds the newly synthetized NIK and induces its ubiquitylation by recruiting of E3 ligases cellular inhibitor of apoptosis (cIAP), needing TRAF2 as an adaptor molecule [44]. Upon activation, the TRAF2–TRAF3–cIAP complex is recruited to the TNFα receptors and its subsequent ubiquitylation and degradation lead to NIK accumulation [44,45]. IKKα is activated by this accumulation independently on trimerization with IKKβ and IKKγ, in contrast to the canonical pathway [46]. Active IKKα ensures the processing of p100 and is followed by translocation of p52–RelB heterodimer into the nucleus to finally modulate NF-κB gene expression [47].

• Rodent studies offer several advantages such as availability of transgenic models that can facilitate mechanistic studies.
• The effects of chronic alcohol exposure are not limited to phenotypic changes in T cells but also include T-cell functions.
• NF-κB is expressed at high levels in microglia and other monocyte-like cells among low levels of innate immune genes in homeostasis.
• 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).
• Vaccines become even more critical as you get older when viruses like RSV and the flu tend to cause more-severe infections, says Dr. Lancaster.

Acetaldehyde is the toxic byproduct that contributes to tissue damage, alcohol dependence, and addiction (Zakhari 2006). It can also bind to other proteins to form adducts, such as malondialdehyde (MDA) and MDA-acetaldehyde (MAA), which play a key role in the development of liver injury and stimulate antibody responses that further promote liver inflammation and fibrosis (Tuma and Casey 2003). In addition, oxidation of ethanol by CYP2E1 leads to the formation of reactive oxygen species (ROS).

How Your Immune System Works

We have long heard about how alcohol can impair our motor skills, judgment, state of consciousness, and, of course, our liver. “Excessive alcohol consumption can cause nerve damage and irreversible forms of dementia,” Dr. Sengupta warns. Your gut microbiome is a hotbed of bacteria that help keep your digestive system happy and healthy. The trillions of microbes in your colon and large and small intestines are critical to proper digestion. “Some people think of the effects of alcohol as only something to be worried about if you’re living with alcohol use disorder, which was formerly called alcoholism,” Dr. Sengupta says.

The presence of ethanol in an in vitro culture of spleen cells also suppressed NK cell cytotoxic activity against MADB106 tumor cells (Yirmiya et al. 1992). Beside the immune cells-mediated host defense, mucous epithelial cells provide a physical barrier and contribute to regulation of innate and as well adaptive immunity. In the last years, microbiota has been extensively studied regarding its impact on various diseases. There is also evidence that alcohol abuse disrupts those epithelial barriers in gastrointestinal and respiratory tracts.