The consequences of impaired gut structural integrity are significant (see figure 1). Chronic drinking — for 12 to 15 years — can lead to a reduction in the number of T cells. Extremely heavy drinking — about 30 drinks per day — can throw off the balance of immune system cells.
“Anything above that, regardless of time period, is exposing your body to more alcohol than is ideal,” says Favini. Examples include certain cancers, as well as pneumonia and other respiratory problems. It can also lead to complications after surgery and poor recovery from injuries such as broken bones.
How Does Alcohol Consumption Affect the Immune System?
That is, by drinking too much, you decrease your body’s defensive mechanisms to fight off a cold, virus, or other bacterial or viral infections. With such conditions, the body’s immune system attacks not only invaders but also its own cells. So if the liver’s immune system is unnecessarily activated due to heavy drinking, it can lead to liver disease.
- An army of antibodies — Another subsystem of the immune system is called adaptive immunity.
- Their main role is to capture, ingest, and process antigens in order to present them on their surface to cells of the adaptive immune response (i.e., to the T-lymphocytes).
- 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.
- 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).
- Rats subjected to chronic alcohol consumption (4 g/kg/day for 12 weeks) exhibit a significant increase in blood pressure compared with controls [188].
- Heavy alcohol use weakens the immune system, and a weak immune system makes it easier to get sick.
Monocytes express Toll-like receptor (TLR) 4, which is the PRR responsible for recognizing the endotoxin LPS on the surface of Gram negative bacteria. Upon LPS binding, monocytes become activated, mature into macrophages and migrate into tissues where they respond to infection by secreting various cytokines, recruiting additional leukocytes via production of chemokines and presenting pathogen-derived peptides to T cells to activate them. Often, investigators stimulate with LPS after pre-exposure to ethanol to mimic inflammation observed in trauma patients with high blood alcohol levels and explore the alterations in immunity that lead to frequent subsequent infections among this group.
Alcohol and HIV Effects on the Immune System
Similarly, more work is needed to determine whether alcohol inhibits specific aspects of B-cell differentiation, such as immunoglobulin class switching and cell survival. These observations suggest that immune defects seen in individuals with AUD could also be mediated by nutritional deficiencies in addition to barrier defects and functional changes in immune cells. However, the contributions of each of these changes to increased susceptibility to infection in individuals with AUD remain to be determined. Alcoholic beverages are energy dense and often become the primary energy source in those with AUD, leading to malnutrition. Individuals with AUD are often deficient in one or more essential nutrients including vitamin A, vitamin C, vitamin D, vitamin E, folate, and thiamine (Hoyumpa 1986). These micronutrients have been shown to play an important role in immune system homeostasis and response to infection (Mora, Iwata et al. 2008).
- When the immune system is down, it is at heightened risk for invasion of disease and infection.
- Mice fed with alcohol (average blood level 139.1 mg/dl) for ten days had higher expressions of mRNA of all TLRs in the liver, except TLR3 and TLR5, while TLR10 and TLR11 were not tested [29].
- Both the innate and the adaptive immune response are critical for effective host defense to infectious challenges.
- Moreover, the wide-ranging roles of the immune system present significant challenges for designing interventions that target immune pathways without producing undesirable side effects.
Much progress has been made in elucidating the relationship between alcohol consumption and immune function and how this interaction affects human health. Normal immune function hinges on bidirectional communication of immune cells with nonimmune cells at the local level, as well as crosstalk between the brain and the periphery. These different layers of interaction make validation of the mechanisms by which alcohol affects immune function challenging. Significant differences between the immune system of the mouse—the primary model organism used in immune studies—and that of humans also complicate the translation of experimental results from these animals to humans. Moreover, the wide-ranging roles of the immune system present significant challenges for designing interventions that target immune pathways without producing undesirable side effects. In addition to pneumonia, alcohol consumption has been linked to pulmonary diseases, including tuberculosis, respiratory syncytial virus, and ARDS.
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
The effects of alcohol on both cell-mediated and humoral immunity have been well-documented since the early 1960s, wherein researchers found that alcohol abuse significantly reduced both CD4 and CD8 T-cell counts. And it’s not just that you’re more likely to get a cold – excessive drinking is linked to pneumonia and other pulmonary diseases. It can also lead to a wide range of health problems, including high blood pressure and does alcohol weaken your immune system heart disease, liver disease, and increased risk of cancer. Alcohol alters the makeup of your gut microbiome – home to trillions of microorganisms performing several crucial roles for your health – and affects those microorganisms’ ability to support your immune system. It seems that drinking alcohol may also damage the immune cells that line the intestines and serve as the first line of defense against bacteria and viruses.
To elicit a response from the cell-mediated arm of the adaptive immunity, antigens need to be presented to the CD4+ and CD8+ T-cells. Studies in rodents found that chronic alcohol feeding can impair presentation of protein antigens in the spleen (Mikszta et al. 1995). Acute alcohol intoxication impairs the antigen-presenting ability of these cells (Mandrekar et al. 2004). In addition, alcohol markedly affects the differentiation of dendritic cells in blood and tissues (Ness et al. 2008). The alcohol-induced defects in dendritic cell function include reduced levels of CD80 and CD86 on the cells’ surface (which are necessary to induce activation of T-cells) as well as reduced production of IL-12, which is critical for stimulating naïve CD4+ T-cells to become IFN-γ–producing Th1 cells. Monocytes and macrophages are leukocytes with a single-lobed nucleus that also act as phagocytes and which therefore also are called mononuclear phagocytes.
Furthermore, another chronic alcohol consumption model underlines a decrease of PMNs chemotaxis after LPS stimulation in alcohol-fed mice [204]. 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 [205]. 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. Additionally, alcohol prevents fMLP-mediated upregulation of CD11b and adhesion efficacy and increases membrane tether length and membrane growth up to three times [205].