Additional evidence for the role of sterile inflammatory signals 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. Alcohol abuse has an adverse effect on hematopoiesis and can cause leukopenia, granulocytopenia, and thrombocytopenia in humans (Latvala et al. 2004).

Gastritis: The Inflammation That Causes Alcohol Bloating

Only if a pathogen can evade the different components of this response (i.e., structural barriers as well as cell-mediated and humoral responses) does the infection become established and an adaptive immune response ensues. Monocytes and macrophages are leukocytes with a single-lobed nucleus that also act as phagocytes and which therefore also are called mononuclear phagocytes. Monocytes are an immature form of these cells that circulate in the blood until they are alerted to the presence of a pathogen in a particular tissue. Once they are at the site of infection, they swell in size and develop into the mature defensive cells—the macrophages—that enter the tissues. After eliminating pathogens by phagocytosis, the monocytes exhibit pathogen-derived proteins and other molecules (i.e., antigens) on their surfaces.

Glucocorticoids sensitize the innate immune system through regulation of the NLRP3 inflammasome

Alcohol affects many organs, including the immune system, with even moderate amounts of alcohol influencing immune responses. Although alcohol can alter the actions of all cell populations involved in the innate and adaptive immune responses, the effect in many cases is a subclinical immunosuppression that becomes clinically relevant only after a secondary insult (e.g., bacterial or viral infection or other tissue damage). Alcohol’s specific effects on the innate immune system depend on the pattern of alcohol exposure, with acute alcohol inhibiting and chronic alcohol accelerating inflammatory responses. The proinflammatory effects of chronic alcohol play a major role in the pathogenesis of alcoholic liver disease and pancreatitis, but also affect numerous other organs and tissues.

• Chronic drinking — for 12 to 15 years — can lead to a reduction in the number of T cells.
• «When you’re feeling run down or like you might get sick, you want to be well hydrated so that all the cells in your body have enough fluid in them and can work really well,» Favini says.
• Similar findings were obtained in animal models, where the number of T cells in the spleen decreased in mice fed a liquid diet (i.e., Lieber-DeCarli diet) containing 7 percent ethanol for as little as 7 days (Saad and Jerrells 1991) or 6 percent ethanol for 28 days (Percival and Sims 2000).
• This increase in circulating Igs correlates with increased levels of antibodies directed against liver antigens and byproducts of oxidative damage.

Impaired immunoglobulin M production by incubation of hybridoma cells with ethanol

• Molecular mechanisms of the dose-dependent effects of alcohol on the immune system and HPA regulation remain poorly understood due to a lack of systematic studies that examine the effect of multiple doses and different time courses.
• «Although there is no evidence that moderate drinking harms the immune system, it is better to stick to wine or beer since these have lower percent alcohol,» Dasgupta says.
• The activities of T-cells and B-cells are intricately intertwined through the actions of various cytokines to orchestrate an effective immune response to any pathogen the organism may encounter.
• It’s important to monitor drinking behavior and consider how it affects health, relationships, and work or school.

The redness and swelling that you see is the result of your body sending more blood to provide nutrients to the site of injury. Alcoholic beverages can cause bloating for various reasons, including the type of drink, carbonation, its ingredients, and anything added to it. Although it may not be possible to avoid bloating and other symptoms after drinking, avoiding drinks that can cause bloating and cutting back on drinking may help.

Effect of alcohol consumption on systemic markers of inflammation

Additional investigations demonstrated that alcohol affects ONP cell differentiation into B lineage at a late stage by down-regulating the expression of several transcription factors (e.g., EBF and PAX5) and cytokine receptors, such as the IL-7 receptor (IL-7Ra) (Wang et al. 2009). In summary, these studies suggest that chronic alcohol abuse in humans and animal models results in lymphopenia, increased T-cell differentiation and activation, and reduced migration (see https://ecosoberhouse.com/ figure 1). Chronic activation of the T-cell pool may alter the T cells’ ability to expand and respond to pathogenic challenges (potentially by inducing a state of unresponsiveness, or anergy, of the T cells), place the T cells under increased regulatory control, or lead to their elimination through increased sensitivity to AICD. These changes in turn compromise the organism’s ability to respond to pathogens and contribute to increased susceptibility to infections.

Another study conducted in humans with self-reported average alcohol consumption of approximately 400 g/day also found an increase in the percentage of both CD45RO+ memory CD4 cells and CD8 cells (Cook et al. 1995). Thus, studies in C57BL/6 mice demonstrated that chronic ethanol consumption (20 percent ethanol in water for up to 6 months) decreased the frequency of naïve T cells and increased the percentage does alcohol weaken your immune system of memory T cells (Song et al. 2002; Zhang and Meadows 2005). 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. Additional analyses detected evidence that T-cell proliferation in the spleen was increased in alcohol-consuming mice (Zhang and Meadows 2005).

Together with TLRs activation, the production of cytokines, which can cross the blood–brain barrier (BBB), have harmful effects at CNS level [102]. Long-term consumption produces serious impairments in the BBB permeability and integrity since alcohol inhibits the expression of BBB structural and functional proteins, promoting inflammation and oxidative stress [107]. In a clinical case study reviewed in this issue, Trevejo-Nunez and colleagues report on systemic and organ-specific immune pathologies often seen in chronic drinkers.

Global and Local Efforts to Take Action Against Hepatitis

Finally, chronic alcohol exposure in utero interferes with normal T-cell and B-cell development, which may increase the risk of infections during both childhood and adulthood. Alcohol’s impact on T cells and B cells increases the risk of infections (e.g., pneumonia, HIV infection, hepatitis C virus infection, and tuberculosis), impairs responses to vaccinations against such infections, exacerbates cancer risk, and interferes with delayed-type hypersensitivity. In contrast to these deleterious effects of heavy alcohol exposure, moderate alcohol consumption may have beneficial effects on the adaptive immune system, including improved responses to vaccination and infection. The molecular mechanisms underlying ethanol’s impact on the adaptive immune system remain poorly understood.

• Gut dysbiosis, which may result in an overgrowth of Gram-negative bacteria [38], can be yielded by the direct toxicity of the alcohol or by indirect mechanisms triggered by alcohol such as the alteration of gut motility [43], the gastric acid output [44], the bile-acid metabolism [45] and an increase in fecal pH [46].
• Studies in rodents found that chronic alcohol feeding can impair presentation of protein antigens in the spleen (Mikszta et al. 1995).
• The large part of alcohol metabolism in humans occurs in the hepatocytes, main cells of the liver.
• Within the GI tract, alcohol exposure can also alter the number and abundance of microorganisms present within the microbiome, all of which play an important role in normal GI function.
• These changes include direct addition of a methyl group to DNA (i.e., DNA methylation) or chemical modifications of the proteins (i.e., histones) around which DNA is wrapped, such as acetylation, methylation, and phosphorylation (Holliday 2006; Hsieh and Gage 2005; Murrell et al. 2005).

The World Health Organization (WHO) and U.S. surgeon general have warned people to avoid drinking too much alcohol during the COVID-19 pandemic. For those who have a risk factor for COVID-19, like heart disease or diabetes, he recommends drinking even less. That said, evidence also shows that even smaller amounts of alcohol can affect the immune system. One study found that people who got less than 7 hours of sleep were nearly three times more likely to develop a cold compared with those who got 8 or more hours of sleep. Drinking also makes it harder for your body to properly tend to its other critical functions, like fighting off a disease.

Impact of AUD on Adaptive Immune Responses

Similarly, more work is needed to determine whether alcohol inhibits specific aspects of B-cell differentiation, such as immunoglobulin class switching and cell survival. The alcohol-related decrease in peripheral B cells primarily seems to be mediated by a decrease in the frequency of the B-2 B cells. The number of B-1a cells also seems to decline, but this decrease is accompanied by a relative increase in the percentage of B-1b cells (Cook et al. 1996). The loss of B-2 cells may explain why alcoholics often cannot respond adequately to new antigens. The relative increase in B-1b cells also may lead to autoantibody production, especially of the IgM and IgA classes (which is discussed below). Catalase is localized to peroxisomes and requires hydrogen peroxide to oxidize alcohol into water and acetaldehyde.