EVs are portrayed as small vesicular structures traversing the extracellular space/bodily fluids. Acetaldehyde is the toxic byproduct that contributes to tissue damage, alcohol dependence, and addiction (Zakhari 2006). It can also bind to other proteins to form adducts, such as malondialdehyde (MDA) and MDA-acetaldehyde (MAA), which play a key role in the development of liver injury and stimulate antibody responses that further promote liver inflammation and fibrosis (Tuma and Casey 2003). In addition, oxidation of ethanol by CYP2E1 leads to the formation of reactive oxygen species (ROS).
Effects on Phagocytic Cells
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). Another study conducted in humans with self-reported average alcohol consumption of approximately 400 g/day also found an increase in the percentage of both CD45RO+ memory CD4 cells and CD8 cells (Cook et al. 1995). Thus, studies in C57BL/6 mice demonstrated that chronic ethanol consumption (20 percent ethanol in water for up to 6 months) decreased the frequency of naïve alcohol and immune system T cells and increased the percentage of memory T cells (Song et al. 2002; Zhang and Meadows 2005).
- In chronically alcohol-fed rats, the T cells fail to proliferate adequately in response to stimulation by IL-2.
- 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).
- Prolonged drug use can cause lasting damage to the immune system, but recovery and healthy habits can help restore its function over time.
CD8+ resident memory T cells
Analyses of alcohol’s diverse effects on various components of the immune system provide insight into the factors that lead to a greater risk of infection in the alcohol-abusing population. This increased susceptibility has been recapitulated in rodent models of chronic alcohol abuse. For instance, increased morbidity and mortality, pulmonary virus titers, and decreased pulmonary influenza-specific CD8 T cell responses were reported in female mice infected with influenza that consumed 20% (w/v) ethanol in their drinking water for 4–8 weeks (Meyerholz, Edsen-Moore et al. 2008). Likewise, higher pathogen burden and decreased CD8 T cell immunity was observed in female mice administered ethanol at 15% (w/v) for 5 days and challenged with Listeria monocytogenes (Gurung, Young et al. 2009). Similar results have been seen in SIV infection of male nonhuman primates (Bagby, Stoltz et al. 2003, Molina, McNurlan et al. 2006, Poonia, Nelson et al. 2006, Marcondes, Watry et al. 2008).
Protective role of light-moderate dose of alcohol in autoimmune diseases
- Excessive alcohol consumption can weaken the immune system, making the body more susceptible to infections.
- Most activated B cells develop into so-called plasma cells, which secrete their antibodies into the blood or lymph.
- Several lines of evidence show that the number and function of B-cells are reduced by chronic alcohol.
Worldwide, tuberculosis (TB) is the leading cause of death from a single infectious agent (Flynn and Bloom 1996). Tuberculosis attacks the lung, https://ecosoberhouse.com/ where immune cells (i.e., macrophages and lymphocytes) battle the infection. In the absence of adequate immunity, however, the bacteria ingested by macrophages continue to multiply within these immune cells, and characteristic lesions called tubercles eventually form in the lungs.
During the intracellular breakdown of the ingested bacteria, the phagocytes generate small proteins or protein fragments that serve as antigens. The phagocytes display these antigens on their cell surface, together with certain of their own proteins known as major histocompatibility complex (MHC) proteins. In addition to the phagocytes, proteins of the complement system also recognize the invading bacteria and bind to proteins on the bacterial surface. This binding triggers several biochemical processes that eventually lead to the destruction of the bacteria. One of the primary ways alcohol affects the immune system is by interfering with the production and function of white blood cells. However, alcohol can impair their ability to function effectively, leaving the body more vulnerable to infections.
Can drug use permanently damage the immune system?
As described earlier for adult humans, alcohol can lead to increases in Ig levels during development, even if the numbers of mature B cells decrease. Thus, maternal alcohol consumption during pregnancy (12 mg/week for most of the pregnancy) increased IgE levels in the umbilical cord blood of the infants (Bjerke et al. 1994). The alcohol-related decrease in peripheral B cells primarily seems to be mediated by a decrease in the frequency of the B-2 B cells. The number of B-1a cells heroin addiction also seems to decline, but this decrease is accompanied by a relative increase in the percentage of B-1b cells (Cook et al. 1996).
Effects on B-Cells
Current research points to health risks even at low amounts of alcohol consumption, regardless of beverage type. The prognosis for individuals with alcohol-related liver failure is often poor without a liver transplant, underscoring the life-altering nature of chronic alcohol misuse. Expression of TNF-α and IL-1β requires the actions of a protein called nuclear factor (NF)- B. Alcohol acts on this molecule (i.e., decreases phosphorylation of I B), thereby allowing I B to attach to NF- B, interfering with its activation of cytokine expression (Mandrekar et al. 1999).
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). Functional medicine evaluates root causes of immune imbalance rather than focusing solely on symptoms. We assess how alcohol interacts with the gut, liver, detox pathways, microbiome, sleep, stress, and nutrient status. Lab testing may reveal markers such as inflammatory cytokines, gut microbiome imbalances, liver enzyme elevations, or altered immune cell profiles.
Roles
After a night of heavy drinking, you might notice that you feel run-down or even come down with a cold shortly thereafter. Acute alcohol consumption can stunt the ability of white blood cells to multiply and respond to pathogens. Even a single episode of binge drinking may reduce the activity of natural killer cells—essential for targeting infected or cancerous cells—for several hours to days. However, it is important to realize that many aspects of alcohol consumption and its effects on immunity and host defense have not yet been fully elucidated.