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. 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. Clinicians have long observed an association between excessive alcohol consumption and adverse immune-related health effects such as susceptibility to pneumonia. As discussed above in the gene expression studies, the mechanisms by which ethanol exerts dose-dependent effects on the immune system could also include modulation of the hypothalamic-pituitary-adrenal (HPA) axis, which tightly regulates the stress response, in turn affecting immunity. Response to different stressors is mediated by several neural circuits that converge on the paraventricular nucleus (PVN) of the hypothalamus (Myers, McKlveen et al. 2014).
- TB can affect any organ system or develop into systemic infection (i.e., miliary TB) when infected cells spread from the lungs and disseminate through the bloodstream.
- Alcohol interferes with the functions of many of the cells and molecules that are part of the immune system.
- 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).
- In the last years, microbiota has been extensively studied regarding its impact on various diseases.
- For example, cultured human monocytes exposed to alcohol showed reduced phagocytic functions; moreover, the cells produced less of a receptor protein that is required for the ingestion of antibody-coated particles.
- Microbiota produces neurotransmitters, tryptophan metabolites, fermentation metabolic by-products such as short-chain fatty acids (SCFAs), the release of cytokines by immune cells and gut hormone signaling.
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). Chronic alcohol consumption also affects the NKT cell populations that play important immunoregulatory roles. 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). In vivo activation of iNKT cells induces a Th1-dominant immune response and enhances the activation of DCs as well as NK cells, B cells, and T cells in alcohol-consuming mice (Zhang et al. 2015).
Can You Mix Prednisone and Alcohol? The Risks of Drinking on Steroids
Chronic alcoholics have impaired T-cell responses; moreover, the balance between Th1 and Th2 responses is shifted toward a predominance of Th2-type responses (Fan et al. 2011; Lau et al. 2006; Szabo 1999). Consistent with this, chronic alcoholics exhibit an increase in IgA and a relative decrease in IgG antibodies, which play a role in antibody-dependent cell-mediated immune responses (Massonnet et al. 2009; Nouri-Aria et al. 1986). Other studies have noted a greater-than-normal abundance of Th17 cells in people with alcoholic liver disease (Lafdil et al. 2010; Ye et al. 2011). For example, even a single dose of alcohol may impair antigen-specific T-cell activation. Thus, in human monocytes and myeloid DCs, alcohol inhibits the cells’ antigen-presentation function as well as their capacity to induce antigen-specific (Mandrekar et al. 2009) and general T-cell activation (Szabo et al. 2001).
Therefore, there is a pressing need for in depth studies that examine dose-dependent effects of chronic ethanol consumption on immunity in vivo to allow for the complex interactions between ethanol, its metabolites, HPA signaling, nutritional deficiencies, and the immune system. In contrast, level of anti-inflammatory protein adiponectin increased (Joosten, van Erk et al. 2012). Similarly, plasma adiponectin concentration was increased after 28 days of daily consumption of 450mL of red wine compared with dealcoholized red wine amongst 34 men, in the absence of changes in subcutaneous and abdominal fat contents as well as body weight (Beulens, van Beers et al. 2006).
Impact of AUD on Lymphocyte Development
The immune response, therefore, would be one of the main channels through which the gut-brain axis establishes communication [108]. Interestingly, central neuroinflammation is maintained after cessation of alcohol consumption, compared to peripheral activation [114] and during periods of abstinence [108]. Finally, in relation to the effect of alcohol on neuroinflammation, a study by Lowe et al. showed an attenuation of alcohol-induced neuroinflammation after reducing the gut bacterial load, as a result of antibiotic treatment [115]. We could hypothesize that by reducing the gut bacterial load, lower amounts of bacterial components would reach the systemic circulation, leading to reduced activation of pro-inflammatory components. 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 figure 1). These changes in turn compromise the organism’s ability to respond to pathogens and contribute to increased susceptibility to infections.
The antibodies are distributed throughout the bloodstream and bind to the bacteria wherever they encounter them, aided by proteins of the complement system. The antibody-covered bacteria clump together and become new targets for monocytes and other phagocytes. T cells circulating in the blood recognize phagocytes simultaneously displaying antigens and MHC proteins. The T cells bind to the phagocyte-bound antigens through the help of docking molecules, called T-cell receptors. The activated T cells multiply and begin secreting cytokines, which, in turn, activate cytotoxic T cells that can then recognize, bind to, and destroy cells infected by the invading bacteria.
Alcohol and Innate Immunity
The main populations of phagocytic cells are composed of monocytes and macrophages, neutrophil granulocytes, and dendritic cells, yet even epithelial, Sertoli cells, or retinal cells provide phagocytosis [151]. 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. “Alcohol has diverse adverse effects throughout the body, including on all cells of the immune system, that lead to increased risk of serious infections,” said Dr. E. Jennifer Edelman, a Yale Medicine addiction medicine specialist. Alcohol abuse represents a risk factor for liver diseases, such as alcoholic steatohepatitis and cirrhosis [37] in such a way that approximately 25% of heavy drinkers develop clinically alcoholic liver disease (ALD).
Alcohol also impairs immune cell function and weakens epithelial barrier function in the lower airways, which can cause bacterial respiratory infections. Gut barrier damage can make the body more vulnerable to food poisoning, and epithelial cell damage can hinder the intestines’ ability to absorb nutrients. When the gut barrier cannot function properly, harmful bacteria can leak into the bloodstream, leading to further complications. Someone who drinks a large number of alcoholic beverages on one occasion or drinks frequently may experience hangover symptoms such as nausea, headache, and dehydration.
Protecting our health
In mice, both short-term and long-term alcohol feeding reduced the phagocytic ability of macrophages residing in the membrane lining the abdominal cavity. Thus, abnormal neutrophil adherence and chemotaxis, as well as reduced phagocytic function of macrophages, may contribute to the impaired defense against microorganisms observed after alcohol consumption. Few studies have investigated the effects of alcohol abuse on complement activation and its relationship with does alcohol weaken your immune system 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). However, alcoholic patients frequently have abnormally low levels of complement in the blood. 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).
It’s not like you can “run around the block one more time” to negate a night of heavy drinking, she said. Another pathway to activate NF-κB is non-canonical signaling, which relies on the tightly-regulated processing of p100, opposed to the rather constant processing of p105 [39]. The canonical NF-κB pathway is responsive to numerous different receptors such as TLR4, IL-1, TNFR, and T-cell receptors [40]. This is in contrast to the non-canonical pathway, which is mostly activated by receptors from the TNFα receptor superfamily [41], including activator of nuclear factor kB [42].