Chronic alcohol consumption decreases the number of circulating T cells, increases the number of activated T cells, accelerates differentiation of T cells to a memory phenotype, and interferes with thymocyte development. A JAMA review of 107 studies published from 1980 to 2021 found that occasional or low-volume drinkers did not have a lower risk of all-cause mortality than lifetime nondrinkers did. But there was a significantly increased risk of mortality among those who had a few drinks per day or more. Alcohol also influences the functions of the lymphoid tissue and alter the activation, secretion, and functions of crucial immune cells called lymphocytes.
Although this chronic weakening of lung function may not cause any immediate symptoms, these effects can manifest when a severe respiratory infection occurs. 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. One of the most common and deadliest conditions afflicting individuals with AUD is bacterial pneumonia. Dr. Benjamin Rush, the first Surgeon General of the United States, described some of the earliest links of alcohol abuse to pneumonia over two centuries ago, reporting that pneumonia was more common in drinkers than nondrinkers (Jellinek 1943; Rush 1810). Two centuries later, the correlation between alcohol abuse and lung infections still remains strong.
Alcohol’s Burden on Immunity Following Burn, Hemorrhagic Shock, or Traumatic Brain Injury
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. There may be important differences in the effects of ethanol on the immune system depending on whether the study is conducted in vitro or in vivo, as the latter allows for a complex psychogenic component in which stress-related hormones and immune-signaling molecules interact. In addition, most studies have been done in vitro using primary cells or cell lines in the presence of rather high, constant doses of ethanol. Similarly, most rodent studies to date have focused on acute/short-term binge models utilizing high concentration of ethanol (20% ethanol) as the sole source of fluid, a possible stressor in itself. 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.
Not only does the immune system mediate alcohol-related injury and illness, but a growing body of literature also indicates that immune signaling in the brain may contribute to alcohol use disorder. The article by Crews, Sarkar, and colleagues presents evidence that alcohol results in neuroimmune activation. This may increase alcohol consumption and risky decisionmaking and decrease behavioral flexibility, thereby promoting and sustaining high levels of drinking.
Can You Be Allergic to Alcohol? Yes, Here’s What to Know About Alcohol Intolerance
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. These observations suggest that immune defects seen in individuals with AUD could also be mediated by nutritional deficiencies in addition to barrier defects and functional changes in immune cells. However, the contributions of each of these changes to increased susceptibility to infection in individuals with AUD remain to be determined.
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. Few studies have investigated the effects of alcohol abuse on complement activation and its relationship does alcohol weaken your immune system with 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.
What happens if your immune system gets too weak?
This NO production stimulates a signaling pathway that involves the enzyme guanylyl cyclase, which produces a compound called cyclic guanosine monophosphate (cGMP). CGMP, in turn, activates cGMP-dependent protein kinase (PKG), followed by activation of the cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA). Activation of this dual kinase signaling pathway results in faster cilia beat frequency (CBF) in cilia briefly exposed to a moderate alcohol dose compared with controls (Sisson 1995; Sisson et al. 2009; Stout et al. 2007; Wyatt et al. 2003). More recent studies demonstrated that this rapid and transient alcohol-induced increase in NO levels was triggered by the alcohol-induced phosphorylation of heat shock protein 90 (HSP90) (Simet et al. 2013b). Upon phosphorylation, HSP90 increases its association with endothelial nitric oxide synthase (eNOS) in cilia, which then activates the cyclase–kinase cascade, resulting in increased CBF (Simet et al. 2013b). These findings are counterintuitive to the conventional wisdom that alcohol interferes with lung host defenses because stimulation of CBF should protect the lung; however, the clinical observation is that heavy alcohol exposure impairs lung host defenses.
They further are characterized by oddly shaped nuclei with multiple lobes and therefore also are called polymorphonuclear leukocytes (PMNs). These cells act as phagocytes—that is, they engulf pathogens and ingest them in a process called phagocytosis. In addition, they can excrete toxic substances from their granules that can kill pathogens. 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).
