Opposing Effects of Alcohol on the Immune System PMC

Chronic alcohol abuse leads to increased susceptibility to bacterial and viral infections, most notably a 3 to 7-fold increase in susceptibility (Schmidt and De Lint 1972) and severity (Saitz, Ghali et al. 1997) of bacterial pneumonia compared with control subjects. Similarly, the incidence of Mycobacterium tuberculosis infection among alcoholics is increased (Sabot and Vendrame 1969, Hudolin 1975, Kline, Hedemark et al. 1995, Panic and Panic 2001). Alcohol use has also been shown to drive disease progression in chronic viral infections such as human immunodeficiency virus (HIV) (Baum, Rafie et al. 2010) and Hepatitis C (Bhattacharya and Shuhart 2003). In addition, the magnitude of antibody response following vaccination with Hepatitis B is lower in alcoholics compared to controls (Nalpas, Thepot et al. 1993). Beyond that, long-term alcohol use leads to the breakdown of the liver or liver failure. Alcohol may also affect an addicted individual’s ability to store adequate amounts of protein.

Higher Vulnerability to Disease

• In vivo studies have confirmed that binge drinking with a blood alcohol concentration (BAC) of approximately 0.4% can reduce the production of various inflammatory cytokines including interleukin-6 (IL-6), IL-10, and IL-12.
• This means that its functioning shifts to focus on breaking down the alcohol and takes its energy from other critical functions such as fighting diseases.
• TLR4-deficient mice prevented such neuroinflammation, synaptic and myelin alterations, as well as long-term cognitive alterations [105].
• Without this defense system, a person is at heightened risk of developing more life-threatening diseases, such as cancer.
• The spike in alcohol sales has alarmed health experts and officials around the world, who are concerned that increased drinking could make people even more vulnerable to the respiratory disease.

[inline_cta_one] The risk to the immune system is not necessarily from drugs or alcohol, but from the toll they take on the body. Many substances cause dehydration, mental or physical does alcohol weaken your immune system fatigue, and lack of food or sleep, which can result in a weakened immune system. When the immune system is down, it is at heightened risk for invasion of disease and infection.

Long-term effects of alcohol misuse

Numerous studies have demonstrated that ethanol, its metabolites, and alterations of the gut microbiome suppress intestinal tight junction protein expression [58,59,60,61] producing that the epithelial layer becomes leaky or “permeable”. Alcohol increased gut permeability affects mucosal immunity and allows the translocation of bacterial or some critical components of their membrane into the bloodstream [47], reaching other organs that can be damaged. LPS (lipopolysaccharide), Gram-negative bacteria membrane main product, and other bacterial metabolites reach the liver https://ecosoberhouse.com/ via the portal vein where they are enabled to induce the activation of the inflammatory processes. A study in rats has shown that only two weeks of alcohol administration disrupts the intestinal barrier and after two weeks more, liver injury occurs [62]. In the liver, gut-derived molecules interact with the hepatocytes, parenchymal cells, and immune cells causing injuries including hepatic steatosis, hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma [63]. This increased susceptibility has been recapitulated in rodent models of chronic alcohol abuse.

Factors That Affect How Alcohol Affects Your Immune System

Whether the increased viral load measured in SIV-infected chronic alcohol-fed macaques can be attributed to diminished CD8+ T-cell function remains to be established (Bagby et al. 2006; Kumar et al. 2005). Both the innate and the adaptive immune response are critical for effective host defense to infectious challenges. Multiple aspects of both arms of the immunity response are significantly affected by alcohol abuse, as described in the following sections. 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). Maintaining gut homeostasis—beneficial microbiota composition—plays a critical role in immune responses.

Effects on CD4+ (Helper) T-Cells

That dual action predisposes heavy drinkers both to increased infection and to chronic inflammation. These articles detail how alcohol affects the immune system and how researchers are harnessing this knowledge to help prevent and treat alcohol-related harm. The first point of contact for alcohol after consumption is the gastrointestinal (GI) system before it is absorbed into the bloodstream. Here, alcohol can damage the epithelial cells, T-cells, and neutrophils in the GI tract, all of which can alter the gut barrier function and allow intestinal microorganisms to leak into circulation.

• For example, the acetaldehyde that is formed during alcohol metabolism can interact with other proteins in the cells, interfering with their function.
• Molina and colleagues review research showing that alcohol impairs recovery from three types of physical trauma—burn, hemorrhagic shock, and traumatic brain injury—by affecting immune homeostasis.
• 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.
• Monocytes and macrophages are leukocytes with a single-lobed nucleus that also act as phagocytes and which therefore also are called mononuclear phagocytes.
• A secondary lung abscess can develop from a lung obstruction or infection that begins in another body part.
• Suppression of inflammatory factors like cytokines is further achieved by the inhibition of histone deacetylases (HDACs) activity.

• Besides in the liver, the enzymes involved in the oxidative metabolism of alcohol also are present in the intestinal mucosa and intestinal bacteria also produce acetaldehyde in the gastrointestinal tract [41].
• Alcohol use can exacerbate mental health conditions, like anxiety and depression, or lead to their onset.
• The induced innate humoral response plays a critical role in clearing or containing infection while an adaptive response develops.
• Once the integrity of the gut mucosa is impaired, LPS enters the portal circulation contributing to enhance the inflammatory changes in other organs such liver and brain.
• “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.

This same treatment also inhibited the in vitro production of IL-6 and IL-12 by peritoneal macrophages harvested 2 hours following injection of LPS (Pruett, Fan et al. 2005). This phenomenon was not observed in a TLR4 mutant mouse, indicating that the acute phase response is mediated by TLR4 (Pruett and Pruett 2006). Alcohol abuse suppresses multiple arms of the immune response, leading to an increased risk of infections. The course and resolution of both bacterial and viral infections is severely impaired in alcohol-abusing patients, resulting in greater patient morbidity and mortality. Multiple mechanisms have been identified underlying the immunosuppressive effects of alcohol.

Molecular Mechanisms of Dose Dependent Modulation of Immunity

Bagby and colleagues review substantial evidence that alcohol further disrupts the immune system, significantly increasing the likelihood of HIV transmission and progression. 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). The PVN regulates pituitary hormone production, including adrenocorticotropic hormone (ACTH), which binds to melanocortin type 2 receptors in the adrenal cortex to induce steroidogenesis in distinct layers (Dringenberg, Schwitalla et al. 2013). Primates have a threelayer adrenal cortex with cortisol being the primary glucocorticoid produced in the zona fasciculata (Nguyen and Conley 2008), which is released in response to stress (O’Connor, O’Halloran et al. 2000). Corticosterone is the main glucocorticoid involved in the regulation of stress responses in rodents (Smith and Vale 2006).

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