It is important to uncover how drinking affects your body’s ability to fight diseases. B cells are characterized by the production of antibodies comprised of Igs. Various types of Igs (e.g., IgA, IgG, IgM) are produced at different times during an infection or in response to a range of antigens that have specific roles in the adaptive immune response. Such studies can be challenging to conduct in humans because of difficulties in obtaining accurate medical histories, maintaining adherence, confounding factors such as diet, sleep-wake cycles, and ethical considerations when studying large doses of ethanol. Rodent studies offer several advantages such as availability of transgenic models that can facilitate mechanistic studies. Rodents have a much shorter life span and often require forced (i.e., not initiated by the animal) exposure to alcohol, which is stressful.
- The severity of a person’s withdrawal symptoms may get worse each time they stop drinking, and can cause symptoms such as tremors, agitation and convulsions (seizures).
- Several studies have also shown that the lungs are highly vulnerable to the effects of alcohol.
- Consuming alcohol likely slows your recovery since your immune system isn’t functioning at optimal levels when you are drinking.
In addition, antigen presenting cells convert vitamin D to 1,25(OH)2VD3, a physiologically active form of vitamin D that is highly concentrated in lymphoid tissues (Mora, Iwata et al. 2008) where it can modulate function of T and B cells which express vitamin D receptors. Vitamin D deficiency results in reduced differentiation, phagocytosis and oxidative burst, by monocytes as well as defective bactericidal activity by keratinocytes (Fabri, Stenger et al. 2011, Djukic, Onken et al. 2014). Alcohol also causes damage to the cells in the outside layer of your stomach and intestines.
What Are the Psychological Effects of Alcohol?
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). Once you start drinking, your body has to work to metabolize the alcohol, since it considers ethanol a toxin. Heavy alcohol use weakens the immune system, and a weak immune system makes it easier to get sick. However, there are signs that you can look for if you are concerned that your drinking might be affecting your immunity. Reducing or quitting drinking can lower alcohol-related damage and improve your overall health.
In addition, chronic alcohol can decrease the number of B-cells that produce an antibody type called IgA5 in one of the layers of mucous membranes (i.e., the lamina propria), which is indicative of altered mucosal immunity (Lopez et al. 1994). Finally, alcohol inhibits the responsiveness of B-cells at certain developmental stages (i.e., blasts, which are the precursors to the antibody-secreting plasma cells) to various cytokines, particularly to IL-2 and IL-4. However, alcohol may have a dual effect on B-cell function because some studies have reported that B-cells also could be activated in alcohol-consuming people (Drew et al. 1984). In addition to these changes in cytokine function, investigators also have shown a contribution of barrier dysfunction to the postinjury increase in infections in intoxicated people (Choudhry et al. 2004). Thus, alcohol intoxication can suppress chemokine production and impair the expression of proteins that allow neutrophils to adhere to other cells at the site of infection, which also contributes to increased susceptibility to infection.
Short-term Effects of Alcohol on the Immune System
It is increasingly evident that sensitization of proinflammatory pathways to activation in monocytes and macrophages after chronic alcohol use has biological and clinical significance. It is known that alcohol-mediated sensitization of immune cells to gut-derived LPS is a major component in the pathogenesis of alcoholic liver disease and alcoholic pancreatitis (Choudhry et al. 2002; Keshavarzian et al. 1994; Nolan 2010; Szabo et al. 2010, 2011). In fact, in acute alcoholic hepatitis, the severity of clinical outcome and death correlates with serum levels of the does alcohol suppress immune system proinflammatory cytokines, particularly TNFα (Frazier et al. 2011; McClain et al. 2004). The exact triggers for alcohol-induced inflammation in the different tissues are yet to be identified. Importantly, deficiency in TLR4, the major sensor of LPS, attenuates inflammation induced by chronic alcohol use in the liver, brain, and intestine (Hritz et al. 2008; Lippai et al. 2013a,b, 2014). However, LPS increase was not found in the brain, suggesting that other ligands and/or alcohol itself may activate TLR4 (Alfonso-Loeches et al. 2010; Lippai et al. 2013b).