Specifically, 24 hours of exposure to both low (1mM) and high (5mM) concentrations of acetaldehyde stimulate IL-6 secretion, however, 7 days of exposure to the high concentration of acetaldehyde, significantly decrease IL-6 secretion (Sarc, Wraber et al. 2011). In contrast, both acute (24 hours) and prolonged (7 days) exposure to low and high concentrations of acetaldehyde reduce TNF-α secretion by primary rat astrocyte (Sarc, Wraber et al. 2011). Monocytes originate from myeloid precursor cells in fetal liver and bone marrow in adult and embryonic hematopoiesis . In brief, the first population constitutes CD14+ cells that are either CD16+ (a receptor for Fcγ of immunoglobulins) or CD16– .
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 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. With such conditions, the body’s immune system attacks not only invaders but also its own cells.
As we said before, your immune system protects your body from unwelcome invaders and certain types of cancers. What’s more, a short period of binge drinking — let’s say a month — can cause a reduction in T cells. 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.
For example, in a model of lung infection, acute alcohol intoxication suppressed the production of certain chemokines (i.e., CINC and MIP-2) during infection and inflammation, thereby markedly impairing the recruitment of additional neutrophils to the site of infection (Boé et al. 2003). This defective neutrophil recruitment could be partially restored by localized chemokine administration (Quinton et al. 2005). The innate cellular response, which is mediated primarily by monocytes/macrophages and does alcohol suppress immune system neutrophils, involves the recognition, phagocytosis, and destruction of pathogens—processes essential to subsequent adaptive responses. Acute and chronic alcohol abuse can interfere with the actions of these cells at various levels. The first line of host defense involves both structural (i.e., epithelial) cells and immune cells (i.e., macrophages and dendritic cells) at mucosal surfaces. The epithelial cells function as a physical barrier as well as regulators of the innate and adaptive immunity.
Leclercq et al.  found a correlation between leaky gut and inflammation with modifications in scores of depression, anxiety and social interactions in alcohol craving. Along the same line, it has been shown that rats replicate several behavioral and biochemical alterations after stool transplantation from patients with depression and anxiety behaviors . In the study of Xiao et al.  transplanted microbiota in mice from alcoholic to healthy, developed emotional symptoms, such as anxiety, which occurs during abstinence. In addition to pneumonia, alcohol consumption has been linked to pulmonary diseases, including tuberculosis, respiratory syncytial virus, and ARDS. Alcohol disrupts ciliary function in the upper airways, impairs the function of immune cells (i.e., alveolar macrophages and neutrophils), and weakens the barrier function of the epithelia in the lower airways (see the article by Simet and Sisson). Often, the alcohol- provoked lung damage goes undetected until a second insult, such as a respiratory infection, leads to more severe lung diseases than those seen in nondrinkers.
Although alcohol is absorbed through the mucosa of the entirely gastrointestinal tract by simple diffusion, it is mainly absorbed in the upper part of the tract , the majority of it (70%) in the small intestine . The large part of alcohol metabolism in humans occurs in the hepatocytes, main cells of the liver. Ethanol is metabolized by alcohol dehydrogenases (ADH), catalase or cytochrome P450 2E1 to acetaldehyde which is then further oxidized to acetate by aldehyde dehydrogenase (ALDH) . Ninety percent of the moderate alcohol consumed is metabolized through oxidative conversion by alcohol dehydrogenases enzymes while the microsomal ethanol–oxidizing system (MEOS) handles the remaining 10%; this last route acquires greater importance when alcohol consumption increases significantly. MEOS leads to the production of oxygen free radicals, which can cause cellular damage .
Treatment with a compound that activates the VDR (i.e., a VDR agonist) restored the T cell’s VDR expression, down-regulated RAS expression as well as ROS generation, and thus preserved T-cell survival (Rehman et al. 2013). They produce immune molecules called antibodies or immunoglobulins that they can either display on their surface or secrete. The antibodies can recognize and interact with antigens, and each B-cell produces antibodies that recognize only one specific antigen. These antibodies then will bind to any matching antigen molecules they encounter in the blood or on other cells, thereby marking them for destruction.
More distinctively, adhesion molecules ICAM-1, VCAM1, and E-selectin, as well as chemokines like CXCL8, MCP-1, and RANTES (“Regulated And Normal T cell Expressed and Secreted”, also known as CCL-5) are significantly reduced . In another model of acute alcohol exposure, injection of 5.5 g/kg alcohol intraperitoneally significantly prevents the E. The authors suggest that E-selectin may play an important role in neutrophil migration . Furthermore, another chronic alcohol consumption model underlines a decrease of PMNs chemotaxis after LPS stimulation in alcohol-fed mice . A further publication shows that alcohol may not only affect the general chemotaxis and migratory behavior of PMNs, but can modulate different steps of neutrophil infiltration in even contrasting directions as well . Here, an in vitro model of alcohol (0.3% by vol.) exposure indicates no effect on PSGL-1, L-selectin, or CD11b expression, but does show altered distribution of PSGL-1 by alcohol.
If you are drinking a lot, stopping or decreasing your alcohol use can also help your chances of not developing severe liver disease. Alcohol can have a range of harmful effects on the body, which can diminish a person’s immune response and put them more at risk for COVID-19. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), moderate drinking is defined as no more than four alcoholic drinks on any single day for men and no more than 14 in total over a week. For women, this reduces to three drinks on any single day and no more than seven drinks over a week. The researchers found that before the monkeys had free access to alcohol, they all demonstrated comparable responses to the vaccinations.
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. 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 . The canonical NF-κB pathway is responsive to numerous different receptors such as TLR4, IL-1, TNFR, and T-cell receptors .
Another study (Rosman et al. 1997) demonstrated that the impaired antibody response in alcoholic patients (i.e., with consumption levels of 230 ± 16 g/day ethanol for 26.4 ± 1.8 years) can be improved by doubling the dose of HepB vaccine from 10 μg to 20 μg at 0, 1, and 6 months. Thus, mice that were chronically fed ethanol generated a weaker antibody response following vaccination with HCV compared with control mice (Encke and Wands 2000). Abstinence partially restored antibody responses against hepatitis antigens in a mouse model (Encke and Wands 2000). In addition to reducing T-cell numbers, chronic alcohol exposure disrupts the balance between different T-cell types (i.e., T-cell homeostasis), leading to a shift toward a memory phenotype. Specifically, people who had consumed 30.9 ± 18.7 alcoholic drinks/day for approximately 25.6 ± 11.5 years exhibited a decreased frequency of naïve (i.e., CD45RA+) CD4 and CD8 T cells, as well as an increased frequency of memory T cells (i.e., CD45RO+) (Cook et al. 1994).