This Is How Alcohol Affects Your Immune System
According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), moderate drinking is defined as no more than four alcoholic drinks on any single day for men and no more than 14 in total over a week. For women, this reduces to three drinks on any single day and no more than seven drinks over a week. The monkeys classed as heavy drinkers showed diminished responses to the vaccine, compared with the monkeys that consumed sugar water.
- Only two studies have examined alcohol-induced changes in colonic (Mutlu, Gillevet et al. 2012) and fecal microbiomes (Chen, Yang et al. 2011), and both studies focused on individuals with AUD.
- As the name implies, helper T cells help control the activity of other immune cells by producing and secreting various cytokines.
- When alcohol is introduced, it damages the lining of organs and certain kinds of white blood cells, disrupts gut barrier function and facilitates bacteria leakage into the rest of the body which can trigger inflammation in the liver.
- The effects of alcohol on both cell-mediated and humoral immunity have been well-documented since the early 1960s, wherein researchers found that alcohol abuse significantly reduced both CD4 and CD8 T-cell counts.
- Your body releases certain proteins that help the immune system, called cytokines, only during sleep.
- Thus, it appears that alcohol inhibits Th1 immune responses and may predispose the organism to Th2 responses and that this shift is at least partly mediated by suppression of IL-12.
Reducing or quitting drinking can lower alcohol-related damage and improve your overall health. If you feel like you cannot control your drinking on your own, you may want to consider seeking addiction treatment. For example, depending on your level of alcohol use, quitting drinking may help resolve the first stage of alcohol liver disease. If you are drinking a lot, stopping or decreasing your alcohol use can also help your chances of not developing severe liver disease. However, chronic and heavy alcohol consumption can lead to fewer T cells and B cells.
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In addition, dysregulation of normal immune responses may contribute to such conditions as alcoholic liver disease and pancreatitis, altered gut permeability and gastrointestinal inflammation, neuroinflammation in the brain, and the development of cancer (see the article by Meadows and Zhang). It is increasingly evident that sensitization of proinflammatory pathways to activation in monocytes and macrophages after chronic alcohol use has biological and clinical significance. It is known that alcohol-mediated sensitization of immune cells to gut-derived LPS is a major component in the pathogenesis of alcoholic liver disease and alcoholic pancreatitis (Choudhry et al. 2002; Keshavarzian et al. 1994; Nolan 2010; Szabo et al. 2010, 2011). 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.
In addition, chronic alcohol can decrease the number of B-cells that produce an antibody type called IgA5 in one of the layers of mucous membranes (i.e., the lamina propria), which is indicative of altered mucosal immunity (Lopez et al. 1994). Finally, alcohol inhibits the responsiveness of B-cells at certain developmental stages (i.e., blasts, which are the precursors to the antibody-secreting plasma cells) to various cytokines, particularly to IL-2 and IL-4. However, alcohol may have a dual effect on B-cell function because some studies have reported that B-cells also could be activated in alcohol-consuming people (Drew et al. 1984). The innate cellular response, which is mediated primarily by monocytes/macrophages and neutrophils, involves the recognition, phagocytosis, and destruction of pathogens—processes essential to subsequent adaptive responses. Acute and chronic alcohol abuse can interfere with the actions of these cells at various levels.
Alcohol distracts the body from other functions
Alcohol abuse has an adverse effect on hematopoiesis and can cause leukopenia, granulocytopenia, and thrombocytopenia in humans (Latvala et al. 2004). Acute alcohol can block differentiation or maturation of granulocytes (i.e., granulopoiesis) during infections (Zhang et al. 2009). Examination of the bone marrow from alcoholic patients has shown vacuolated granulopoietic progenitors with a significantly reduced number of mature granulocytes (Yeung et al. 1988). Alcohol intoxication also can suppress the myeloid proliferative response by inhibiting the Stem Cell Antigen-1/ERK pathway during bacterial infection (Melvan et al. 2012).
For example, a 2015 study in the journal Alcohol found that binge drinking can reduce infection-fighting white blood cells known as monocytes in the hours after peak intoxication, essentially weakening your immune system. And it’s not just that you’re more likely to get a cold — excessive drinking is linked to pneumonia and other pulmonary diseases. It can also lead to a wide range of health problems, including high blood pressure and heart disease, liver disease, and increased risk of cancer. “By damaging those cells in your intestines, it can make it easier for pathogens to cross into your bloodstream,” says Nate Favini, MD, medical lead at Forward, a preventive primary care practice. 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.
Long-term effects of alcohol on the immune system
A weak immune system can put you at higher risk of various medical conditions. As we said before, your immune system protects your body from unwelcome invaders and certain types of cancers. Fortunately, not drinking for 30 days can bring T cell counts back to normal https://ecosoberhouse.com/ levels. They do this by destroying the cells in your body that have been taken over by viruses. When you have an illness or get a vaccine, your body’s B cells create antibodies. These antibodies attack invaders and prevent an infection from spreading further.
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. “Alcohol intake can kill normal healthy gut bacteria, which help to promote health and reduce risk of infection,” Mroszczyk-McDonald said. When someone is exposed to a virus, the body mounts an immune response to attack and kill the foreign pathogen. Soon after, the World Health Organization (WHO) also suggested that people cut back on drinking, since alcohol can increase the risk of experiencing complications from COVID-19. The study researchers, led by Ilhem Messaoudi of the School of Medicine at the University of California, Riverside, say their research may help lead to a better understanding of how the immune system works, and how to improve its ability to respond to vaccines and infections.
Modulation of Innate Immunity by Alcohol
Beyond a very small amount, though, there is a sharp upswing of negative impacts—a J-shaped curve,” she says. Biomedical consequences of alcohol-induced dysregulation of the immune system. These may include infections after surgery, traumatic injury, or burns; accelerated progression of HIV disease; adult respiratory distress syndrome and other opportunistic lung infections; and infection with hepatitis C virus, cirrhosis, or liver cancer (hepatocellular carcinoma). https://ecosoberhouse.com/article/does-alcohol-weaken-our-immune-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. Therefore, it is possible that acetaldehyde also interacts with antibodies and thereby may alter antibody responses; however, this remains to be established (Thiele et al. 2008).
- Mandrekar and Ju contribute an article that homes in on the role of macrophages in ALD development, including recent insights into the origin, heterogeneity, and plasticity of macrophages in liver disease and the signaling mediators involved in their activation and accumulation.
- Drinking also makes it harder for your body to properly tend to its other critical functions, like fighting off a disease.
- Then, take the next dose after your regularly scheduled number of hours have passed.
- Finally, an emerging informatics approach that can piece together these extensive data sets and build a network between the immune response elements, the HPA axis, and the time-course/dose response of ethanol while emphasizing in vivo studies from rodent, non human primate, and humans is urgently required.
- The inflammasome is a multiprotein intracytoplasmic complex that comprises a sensor (e.g., NLRP1, NLRP3, NLRC4, or a protein called AIM2) and adapter molecules (e.g., a molecule called ASC).
- 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.
- 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).
Clinicians have long observed an association between excessive alcohol consumption and adverse immune-related health effects such as susceptibility to pneumonia. Several lines of evidence show that the number and function of B-cells are reduced by chronic alcohol. For example, chronic alcoholics exhibit loss of B-cells in the periphery and a reduced capacity to generate protective antibodies (Cook et al. 1996).
These receptors recognize viral nucleic acids (i.e., DNA and RNA) and mount an immediate response mediated by interferons (Stetson and Medzhitov 2006; Takeuchi and Akira 2009). Production of interferons in monocytes is induced by activation of various TLRs and helicase receptors. The actions of interferons within the cells, in turn, are mediated by regulatory molecules called signal transducers and activators of transcription (STATs), a family of transcription factors that regulate the expression of certain immune genes. Thus, both acute and chronic alcohol inhibit induction of Type-I interferons via TLR3, TLR7/8, or TLR9 or by helicase receptors in monocytes (Pang et al. 2011; Pruett et al. 2004). Alcohol also impairs Type-I interferon-receptor signaling by inhibiting STAT signaling (Norkina et al. 2008; Plumlee et al. 2005).