How Alcohol Weakens the Immune System

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). These molecules enter the circulation to the liver where they activate endothelial and stellate cells as well as hepatocytes, resulting in a chronic inflammatory environment aggravating organ injury. T and B cell activation in the presence of retinoic acid results in the up-regulation of gut-homing molecules and generation of IgA-secreting B cells (Mora, Iwata et al. 2008).

  • For example, the pattern of alcohol consumption (e.g., occasional binge drinking versus chronic heavy drinking) may affect the immune system in different ways that are yet to be explored.
  • 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).
  • The Centers for Disease Control and Prevention (CDC) also advise people who do not currently drink to avoid starting for any reason.
  • The issue of leukocyte migration in the presence of alcohol as well as pathogens is a common sight every day in clinical practice.
  • The association between genetically predicted levels of alcohol consumption and risk of common autoimmune inflammatory diseases.

In addition to promoting proinflammatory immune responses, alcohol also impairs anti-inflammatory cytokines. Chronic alcohol exposure also interferes with the normal functioning of all aspects of the adaptive immune response, including both cell-mediated and humoral responses. All of these effects enhance the susceptibility of chronic alcoholics to viral and bacterial infections and to sterile inflammation. Cytokines are affected by alcohol on several levels as they are induced by certain pathways affected by alcohol, which again, in turn, can be modulated by other cytokines. Summarized, this makes it difficult to differentiate between altered cytokine actions and altered cytokine release. In an in vitro model of acute inflammation, pretreatment of human lung epithelial cells with alcohol (85 or 170 mM) for 24 or 72 hours reduces IL-8 release upon their stimulation with IL-6.

Macrophages and Alcohol-Related Liver Inflammation

The redness and swelling that you see is the result of your body sending more blood to provide nutrients to the site of injury. According to the Cleveland Clinic, once you take a sip of alcohol, your body prioritizes breaking down alcohol over several other bodily functions. The body doesn’t have a way to store alcohol like it does with carbohydrates and fats, so it has to immediately send it to the liver, where it’s metabolized.

does alcohol suppress immune system

It is now thought that alcohol-induced sterile danger signals contribute to the proinflammatory cytokine activation seen after chronic alcohol use in various organs (e.g., liver, intestine, and brain). This hypothesis also is supported by findings that in hepatocytes, alcohol exposure results in a rapid induction of apoptosis, which precedes induction of inflammatory cytokines (Caradonna et al. 2000; González-Reimers et al. 2014; Marchettia et al. 2013; Petrasek et al. 2013). Additional evidence for the role of sterile inflammatory signals does alcohol suppress immune system in alcohol-induced inflammation and tissue damage comes from findings that HMGB1 is increased both in the liver and brain after chronic alcohol exposure (Crews et al. 2013; Csak et al. 2014; Lippai et al. 2013a,b). Finally, NLRs, specifically NLRP3 and NLRP4, have been found to be involved in alcoholic liver inflammation. Given the role of NLRs in sensing endogenous danger molecules, this observation further supports the notion that alcohol-induced tissue inflammations is caused at least partially by alcohol-induced danger signals.

Is There Any Amount of Alcohol That’s OK to Drink?

These adaptive immune cells include T cells, B cells, and natural killer T cells (NKTs), which must cooperate in a controlled manner to mount an effective response (Castellino and Germain 2006; Mitchison 2004). T cells in turn fall into several different categories, including helper T cells, also known as CD4+ cells; cytotoxic T cells, also called CD8+ cells; Th17 cells; and regulatory T (Treg) cells (table 1). As the name implies, helper T cells help control the activity of other immune cells by producing and secreting various cytokines. Following chronical excessive alcohol intake, the intestinal barrier becomes “leaky” by altered tight junctions of epithelial cells. On the one hand, alcohol impairs the trafficking of zona occludens (ZO)-1 and occludin, both proteins of tight junctions [209].

  • A second study by Joosten et al. also analyzed gene expression profiles in PBMCs isolated from 24 healthy male subjects who consumed 50mL of vodka with 200mL orange juice or only orange twice daily for 4 weeks during dinner (considered to be moderate).
  • Alcohol consumption does not have to be chronic to have negative health consequences.
  • Chronic alcohol consumption in humans causes alterations in the immunophenotype of DCs and decreased production of IL-1β and TNFα (Laso et al. 2007).
  • 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).
  • 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).

Stress, poor diet, food allergies, chemotherapy and other medication, conditions such as inflammatory bowel disease and — perhaps crucially — overuse of alcohol can damage the layer of epithelial cells that line the intestines. This can make the intestinal wall permeable to food particles and bacteria, which can then sneak into the circulatory system. Despite these observations, which shed some light on alcohol’s effects on B-cells and their functions, some questions remain to be answered. For example, the acetaldehyde that is formed during alcohol metabolism can interact with other proteins in the cells, interfering with their function.

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