If you’re unfamiliar, inflammation is what naturally occurs when your immune system goes into action. 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. 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.
In addition, the blood is merely a “window” reflecting only a small part of the immune system as a whole, and the effects of mucosal barrier damage and inflammation may not be adequately reflected in monitoring peripheral blood alone. 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.
Does Alcohol Interact With HIV?
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). In conclusion, alcohol can enable pathogens to enter the systemic blood flow, a process that may lead to an increased susceptibility of patients with infections. does alcohol suppress immune system Furthermore, the induction of DAMPs in a sterile environment by alcohol should be a focus of further research, because, potentially, this may provide novel understanding of the chronic inflammation after alcohol consumption in case of no visible damage to organs. There is evidence in a number of physiological systems that binge alcohol intake complicates recovery from physical trauma (see the article by Hammer and colleagues).
Similarly to the intestine, the lung epithelial barrier is affected by chronical alcohol abuse as well, contributing to the pathophysiology of acute respiratory distress syndrome or acute lung injury. The interference of the granulocyte/macrophage colony stimulating factor signaling inhibits the macrophage maturation needed for maintenance of epithelial barrier integrity , and the bronchial epithelium ciliary function required for mechanical bacteria clearance has also been reported to be impaired . Although most research has focused on the effects of heavy alcohol consumption on the immune system, several studies have also confirmed that even moderate consumption can have significant effects on the immune system. For example, one study found that women who consumed 330 mL of beer for 30 days exhibited a significant increase in leukocytes, mature CD3+ T-cells, neutrophils, and basophils. In contrast, men who consumed a similarly moderate amount of beer for the same period exhibited a significant increase in basophils alone. The immune system is typically categorized into the innate and adaptive immune response systems, both of which are essential components in the body’s defense against pathogens.
The Adaptive Immune Response
In conclusion, the evidence for alcohol to greatly influence cytokine production is indisputable. Further clinical studies using healthy subjects will point to certain cytokines that may be usable as biomarkers for alcohol disease or for its immuno-modulatory impact. Catalase is localized to peroxisomes and requires hydrogen peroxide to oxidize alcohol into water and acetaldehyde.
This part of the immune response is specific to one particular pathogen and also creates an “immune memory” that allows the body to respond even faster and more effectively if a second infection with the same pathogen occurs. Thus, both types of immunity are mediated partly by the actions of specific immune cells (i.e., include a cell-mediated response) and partly by the actions of molecules secreted by various immune cells (i.e., include a humoral response). It is also critical to take into consideration that the effects of ethanol on immune function in vivo could involve the actions of its primary metabolite, acetaldehyde. Therefore, more studies looking at the effects of ethanol metabolites in vivo are needed. Acetaldehyde has also been shown to affect NFκB-induced cytokine production in various liver cells.
One study found that alcohol increases the percentages of memory CD4+ T cells in the gut, suggesting that alcohol use may increase turnover of viral target cells in intestinal tissues (Poonia et al. 2006). Although the mechanisms behind this still are under investigation, it is possible that repetitive damage to the intestinal epithelium by alcohol may simply result in chronic inflammation, which recruits these T cells to the intestine through the above pathways. Thus, alcohol use in HIV infection may result in increased turnover of viral target cells in the intestine, which may partially explain why macaques infected with SIV have significantly higher levels of viremia in primary SIV infection (Bagby et al. 2006; Poonia et al. 2005). 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).