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6 Ways Alcohol Affects Your Health

The loss of B-2 cells may explain why alcoholics often cannot respond adequately to new antigens. The relative increase in B-1b cells also may lead to autoantibody production, especially of the IgM and IgA classes (which is discussed below). The white blood cells, tissues and organs that make up our body’s immune system are designed to fight off infections, disease and toxins. Gut microbiota are able to produce various of the aforementioned metabolites that act on enteroendocrine cells, the vagus nerve or by translocation throughout the gut epithelium into the systemic circulation and may have an impact on host physiology.

Each of these events is mediated by the activation of nuclear factor kappa B (NFκB), which can be inhibited by alcohol consumption and thus prevent the production of pro-inflammatory cytokines. 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 the best gifts for celebrating 1-year sobriety cytokines including interleukin-6 (IL-6), IL-10, and IL-12. These results could support a role, via an anti-inflammatory mechanism, for moderate alcohol intake in cardiovascular disease (CVD) prevention. This outcome underscores the importance of taking into account the amount of alcohol consumption when evaluating the immune response.

Interestingly, chronic alcohol abuse causes leaky gut-dependent malabsorption in the small intestine that is comparable with untreated celiac disease [213]. Further, despite the increased intestinal permeability, bacterial overgrowth and compositional disbalance has been described. Patients with chronic alcohol overconsumption show lowered counts of protective gastrointestinal bacteria such as Lactobacillus, Faecalibacterium, or Bacteroidetes, whereby the pathogenic bacterial families such as Proteobacteria, Enterobacteriaceae, and Streptococcaceae were overrepresented [214].

  1. In addition, alcohol significantly inhibits PMN phagocytic activity as well as the production or activity of several molecules (e.g., superoxide or elastase) that are involved in the PMNs’ bactericidal activity (Stoltz et al. 1999), so that overall bactericidal activity ultimately is reduced.
  2. The number of B-1a cells also seems to decline, but this decrease is accompanied by a relative increase in the percentage of B-1b cells (Cook et al. 1996).
  3. Moreover, the wide-ranging roles of the immune system present significant challenges for designing interventions that target immune pathways without producing undesirable side effects.
  4. These disruptions to the composition of the gut microbiota and to gut barrier function have important implications beyond the intestinal system.

These mechanisms involve structural host defense mechanisms in the gastrointestinal and respiratory tract as well as all of the principal components of the innate and adaptive immune systems, which are compromised both through alcohol’s direct effects and through alcohol-related dysregulation of other components. 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. These disruptions to the composition of the gut microbiota and to gut barrier function have important implications beyond the intestinal system. For example, Nagy discusses how the leakage of bacterial products from the gut activate the innate immune system in the liver, triggering inflammation that underlies ALD, a condition that affects more than 2 million Americans and which eventually may lead to liver cirrhosis and liver cancer. Infection with viral hepatitis accelerates the progression of ALD, and end-stage liver disease from viral hepatitis, together with ALD, is the main reason for liver transplantations in the United States.

Active IKKα ensures the processing of p100 and is followed by translocation of p52–RelB heterodimer into the nucleus to finally modulate NF-κB gene expression [47]. Additionally, IKKα phosphorylates NIK and is thereby regulating itself via a negative feedback loop [47]. 4Expression of TNF-α and IL-1β requires the actions of a protein called nuclear factor (NF)- B. The activity of this protein is regulated by another molecule, inhibitor of NF- B (I 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). In addition, alcohol interferes with TNF expression by inhibiting the normal processing of newly produced TNF that is necessary for normal TNF functioning (Zhao et al. 2003).

The adaptive immune system is highly specific to a particular pathogen and is formed by B and T cells lymphocytes. (B) The gut microbiota is in close interaction with both the innate and the adaptive immune system. This interaction is frequently driven by SCFAs, which modulate local as well as systemic immune response.

Moderate alcohol consumption and the immune system: a review

IgA concentrations also were increased in a layer (i.e., the lamina propria) of the mucous membranes lining the intestine of adult female Wistar rats after acute ethanol administration (4g/kg intraperitoneally) for 30 minutes (Budec et al. 2007). Recent studies suggest that the increase in IgA levels may be mediated by an ethanol- induced elevation of the enzyme neuronal nitric oxide synthase (nNOS) in the animals’ intestine, because inhibition of nNOS before ethanol injection suppressed the IgA increase (Budec et al. 2013). However, additional studies are needed to fully uncover the mechanisms that underlie increased Ig production while B-cell numbers are reduced.

Additionally, alcohol prevents fMLP-mediated upregulation of CD11b and adhesion efficacy and increases membrane tether length and membrane growth up to three times [205]. Interestingly, the rolling velocity is also reduced by 55% compared to control cells [205]. In male Sprague-Dawley rats which have been nourished with Sustacal liquid diet (Mead Johnson, Evansville, IN) supplemented with 36% alcohol for four months, PMNs isolated from blood samples have upregulated CD18 expression on neutrophils to double that of control rats [206]. (A) The innate immune response is a very fast, pathogen-non-specific, first line of defense mechanism. It is mainly composed of macrophages, dendritic and natural killer cells, as well as different forms of granulocytes.

Impact of AUD on T Cells

Potential intracellular target points for (i) acute alcohol and (ii) chronic alcohol in a stylized cell. The induction of canonical NF-κB with p50–p65 translocation to nucleus via pattern recognition receptors (PRR) is outlined by, for example, TLR4 and MyD88 activation. The non-canonical NF-κB pathway with p52-RelB is detailed with CD40 as the respective receptor.

In animal models, the consumption of ethanol only led to lower levels of white blood cells; however, the same amount of alcohol consumed as red wine resulted in no suppression of the immune response. This could be due to the action of certain compounds in red wine that could be contributing to prevent suppression of the immune system caused by alcoholReference Percival and Sims27. Similarly, wine intake, especially red wine, has been identified as having a protective effect against the common coldReference Takkouche, Regueira-Mendez, Garcia-Closas, Figueiras, Gestal-Otero and Hernan29. Daily moderate consumption of alcohol (500 ml of a 12 % ethanol dilution), and 500 ml of red wine, red grape juice, and dealcoholised red wine for 2 weeks at doses which inversely correlate with CVD risk did not show any effects on human immune cell functionsReference Watzl, Bub, Pretzer, Roser, Barth and Rechkemmer30. However, the design of this study could be questioned since the duration may have been insufficient to affect the immune system; probably it would take up to six weeks to see changes and differences in the immune system. Beside the immune cells-mediated host defense, mucous epithelial cells provide a physical barrier and contribute to regulation of innate and as well adaptive immunity.

Understanding alcohol and our immune system

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). 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. Clinicians have long observed an association between excessive alcohol consumption and adverse immune-related health effects such as susceptibility to pneumonia. Taken together, all these findings suggest that in utero exposure to ethanol may increase the risk for infections during early childhood or adulthood as a result of alcohol-induced defects in B-cell and T-cell development. Indeed, in utero exposure to ethanol resulted in a significant reduction in T-cell and B-cell responses to various antigens that did not recover to control levels until 4 to 5 weeks of life.

Alcohol and Structural Host Defense Mechanisms

Naïve human T cells produce low levels of VDR, but expression is increased to moderate levels in activated T cells (Irvin et al. 2000). Human T cells incubated in vitro with variable concentrations of ethanol (0, 10, 25, and 50mM for 24 hours) showed a reduced expression of the VDR, accompanied by increased expression of RAS and ROS as well as increased T-cell death (Rehman et al. 2013). Additional analyses demonstrated expressive arts therapy that ethanol exposure promoted apoptosis by inducing breaks in the DNA of the T cells. This damage to the DNA most likely was mediated by ROS generation in response to RAS activation. 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).

Monocytes originate from myeloid precursor cells in fetal liver and bone marrow in adult and embryonic hematopoiesis [152]. In brief, the first population constitutes CD14+ cells that are either CD16+ (a receptor 4 ways to make amends in recovery for Fcγ of immunoglobulins) or CD16– [153]. While these monocyte populations can differentiate into macrophages or dendritic cells and augment tissue macrophages, they do not replenish tissue macrophages [155].

How Alcohol Can Affect Your Immune System

There is evidence in a number of physiological systems that binge alcohol intake complicates recovery from physical trauma (see the article by Hammer and colleagues). 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. Their article also highlights how the combined effect of alcohol and injury causes greater disruption to immune function than either challenge alone. The gastrointestinal (GI) system is typically the first point of contact for alcohol as it passes through the body and is where alcohol is absorbed into the bloodstream.

Only if a pathogen can evade the different components of this response (i.e., structural barriers as well as cell-mediated and humoral responses) does the infection become established and an adaptive immune response ensues. The ability of alcohol to alter both innate and adaptive immune defenses inevitably impacts how the immune system of even a moderate alcohol drinker can respond to infections. In fact, alcohol use has been shown to increase the susceptibility of drinkers to both bacterial and viral infections, as well as advance the progression of several chronic viral infections, including human immunodeficiency virus (HIV) and hepatitis C.

Integrating gene expression patterns with gene regulation could reveal novel insight into specific pathways that are dysregulated with alcohol abuse and could explain the increased susceptibility to infection. These insights could lead to interventions to restore immunity, such as reversing changes in histone modifications and DNA methylation patterns or modulating expression levels of miRNAs. In addition, such studies could reveal the pathways that are modified by moderate alcohol consumption to enhance immune response to vaccination. The issue of leukocyte migration in the presence of alcohol as well as pathogens is a common sight every day in clinical practice. In a prospective clinical study of precariously ill non-trauma patients, those individuals who were acutely intoxicated with alcohol have markedly diminished quantities of CRP, circulating neutrophils, and neutrophil CD64 indices [200].