Some of these mechanisms are directly related to the pathology found in people with infections such as HIV/AIDS, tuberculosis, hepatitis, and pneumonia who continue to use and abuse alcohol. These mechanisms involve structural host defense mechanisms in the gastrointestinal and respiratory tract as well as all of the principal components of the innate and adaptive immune systems, which are compromised both through alcohol’s direct effects and through alcohol-related dysregulation of other components. Analyses of alcohol’s diverse effects on various components of the immune system provide insight into the factors that lead to a greater risk of infection in the alcohol-abusing population. 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). Recent studies suggest that the increase in IgA levels may be mediated by an ethanol- induced elevation of the enzyme neuronal nitric oxide synthase (nNOS) in the animals’ intestine, because inhibition of nNOS before ethanol injection suppressed the IgA increase (Budec et al. 2013). In addition, production of IL-10 in response to TLR2/6 stimulation was increased (Pruett, Zheng et al. 2004).
Alcohol’s Burden on Immunity Following Burn, Hemorrhagic Shock, or Traumatic Brain Injury
Heavy drinking can also lead to a host of health concerns, like brain damage, heart disease, cirrhosis of the liver and even certain kinds of cancer. Alcohol–immune interactions also may affect the development and progression of certain cancers. Meadows and Zhang discuss specific mechanisms through which alcohol interferes with the body’s immune defense against cancer. They note, too, that a fully functioning immune system is vital to the success of conventional chemotherapy.
Impact of Alcohol Abuse on the Adaptive Immune System
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). Chronic alcohol consumption reduces B-cell numbers, decreases does alcohol weaken your immune system antigen-specific antibody responses, increases the production of auto-antibodies, and interferes with B-cell development and maturation. Chronic excessive alcohol consumption causes inflammation in a variety of organs, including the gut, brain and liver. While alcohol has direct effects on the gastrointestinal tract when it comes into touch with the mucosa, the majority of alcohol’s biological effects are due to its systemic dispersion and delivery through the blood.
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In fact, in acute alcoholic hepatitis, the severity of clinical outcome and death correlates with serum levels of the proinflammatory cytokines, particularly TNFα (Frazier et al. 2011; McClain et al. 2004). The exact triggers for alcohol-induced inflammation in the different tissues are yet to be identified. Importantly, deficiency in TLR4, the major sensor of LPS, attenuates inflammation induced by chronic alcohol use in the liver, brain, and intestine (Hritz et al. 2008; Lippai et al. 2013a,b, https://ecosoberhouse.com/ 2014). However, LPS increase was not found in the brain, suggesting that other ligands and/or alcohol itself may activate TLR4 (Alfonso-Loeches et al. 2010; Lippai et al. 2013b). The human gut is the largest organ with immune function in our body, responsible for regulating the homeostasis of the intestinal barrier. A diverse, complex and dynamic population of microorganisms, called microbiota, which exert a significant impact on the host during homeostasis and disease, supports this role.
The Gastrointestinal Microbiome: Alcohol Effects on the Composition of Intestinal Microbiota
That is, by drinking too much, you decrease your body’s defensive mechanisms to fight off a cold, virus, or other bacterial or viral infections. With such conditions, the body’s immune system attacks not only invaders but also its own cells. So if the liver’s immune system is unnecessarily activated due to heavy drinking, it can lead to liver disease. 4Similarly, chronic consumption of 18 percent ethanol in water for 31 weeks resulted in impaired antigen-specific CD8 T-cell responses following inoculation with Listeria monocytogenes (Gurung et al. 2009). 1T-cell activation was assessed by measuring the expression of human leukocyte antigen (HLA)-DR on the patient’s CD8 cells. HLAs are proteins found on the surface of various cells that present antigens to the TCR on T cells to induce an immune response.
Alcohol-Induced Modulation of the Host Defense Against Different Pathogens
- Thus, alcohol consumption enhances immature NKT (iNKT) cell proliferation and maturation in the thymus and increases IFN-γ–producing iNKT cells (Zhang et al. 2015).
- Alcohol can have a range of harmful effects on the body, which can diminish a person’s immune response and put them more at risk for COVID-19.
- In addition to producing proinflammatory cytokines, innate immune cells (particularly DCs and monocytes) are necessary to present pathogen-derived molecules (i.e., antigens) to adaptive immune cells so as to trigger or facilitate adaptive immune responses.
- These membranes line the body cavities exposed to the external environment (e.g., the GI tract, respiratory tract, nostrils, mouth, or eyelids) and therefore are likely to come in contact with outside pathogens.
- Vitamin E is one of the most effective antioxidants and its deficiency exacerbates freeradical damage impairing the ability of T cells to respond to pathogenic challenge (Mocchegiani, Costarelli et al. 2014).
Thus, alcohol intoxication can suppress chemokine production and impair the expression of proteins that allow neutrophils to adhere to other cells at the site of infection, which also contributes to increased susceptibility to infection. For example, in a model of lung infection, acute alcohol intoxication suppressed the production of certain chemokines (i.e., CINC and MIP-2) during infection and inflammation, thereby markedly impairing the recruitment of additional neutrophils to the site of infection (Boé et al. 2003). This defective neutrophil recruitment could be partially restored by localized chemokine administration (Quinton et al. 2005).
- PMNs produce a host of bacteria-killing (i.e., bactericidal) molecules (e.g., myeloperoxidase, defensins, azurophil-derived bactericidal factors, bactericidal permeability-increasing protein, cationic proteins, gelatinase, and lactoferrin).
- This effect may contribute to lung injury in response to inflammation (Holguin et al. 1998).
- Changes persisted at least 30 days after alcohol exposure suggestive of longlasting consequences of ethanol on microglia function (McClain, Morris et al. 2011).
- DCs, which are the major cell type linking the innate and adaptive immune response, also are affected by alcohol intoxication.
- Gut microbiota are able to produce various of the aforementioned metabolites that act on enteroendocrine cells, the vagus nerve or by translocation throughout the gut epithelium into the systemic circulation and may have an impact on host physiology.
What Are the Immediate and Long-Term Health Benefits After You Stop Drinking Alcohol?
- This loss of naïve T cells could result from decreased T-cell production in the thymus; increased cell death (i.e., apoptosis) of naïve T cells; or increased homeostatic proliferation.
- These antibodies then will bind to any matching antigen molecules they encounter in the blood or on other cells, thereby marking them for destruction.
- Similarly, as with the Th1 responses, alcohol inhibits the ability of dendritic cells to promote Th17 responses, thereby favoring Th2 responses (Heinz and Waltenbaugh 2007).
- The PVN regulates pituitary hormone production, including adrenocorticotropic hormone (ACTH), which binds to melanocortin type 2 receptors in the adrenal cortex to induce steroidogenesis in distinct layers (Dringenberg, Schwitalla et al. 2013).
- Together, they provide valuable insights into the challenges, successes, and the importance of partnerships in the fight against hepatitis.
- SCFAs produced in the gut are mainly butyrate, propionate and acetate and have many different targets and functions in the host organism.
- The studies found that when animals consumed ethanol before BCG vaccination, they were not protected against a subsequent pulmonary challenge with M.
- The gut-derived bacterial components together with LPS activate the immune cells localized in the systemic circulation or in target organs such as liver and brain.
- In such patients, alcohol impairs mucosal immunity in the gut and lower respiratory system.
- This increased susceptibility has been recapitulated in rodent models of chronic alcohol abuse.