The respective study design is mentioned as well as the investigated cells/compartments and limitations to help the reader classify the given information. Alcohol abuse suppresses multiple arms of the immune response, leading to an increased risk of infections. The course and resolution of both bacterial and viral infections is severely impaired in alcohol-abusing patients, resulting in greater patient morbidity and mortality. Multiple mechanisms have been identified underlying the immunosuppressive effects of alcohol. 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.
In patients admitted to hospital with acute alcoholic hepatitis, serum levels of IL-8, IL-4, and IFNγ are higher than age- and sex-matched control patients [132]. The severity of this alcohol-induced hepatitis directly correlates with cytokine concentration, yet they can normalize after recovery [133]. 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]. The capability of neutrophils to roam blood vessels in order to find inflammation spots is not only crucial to the innate immune system but also visible in the expression of aforementioned adhesion molecules [196]. In a carrageenan air pouch model of mice subjected to bolus injection of alcohol (1.5 g/kg) and with LPS (1 ug/mL) afterward, the expression of adhesion molecules was investigated [201].
Structural Responses
Reducing or quitting drinking can lower alcohol-related damage and improve your overall health. Fortunately, not drinking for 30 days can bring T cell counts back to normal levels. Your immune system has several different cell types, each of which has a different but very important job to help keep you healthy. “Those at increased risk should cut down or abstain from alcohol because every little thing an individual can do to improve the health and reduce risk is worth it at this point, even if the evidence is not entirely clear,” Mroszczyk-McDonald said. When someone is exposed to a virus, the body mounts an immune response to attack and kill the foreign pathogen.
- Moreover, significant dysregulation of genes critically involved in wound healing, blood coagulation, cancer, cardiovascular, and lung diseases was shown in chronic heavy drinkers [51,52].
- Several lines of evidence suggest that alcohol consumption exerts a dose-dependent impact on the host response to infection.
- “Anyone with chronic liver conditions should be avoiding alcohol, for example, people with hepatitis, nonalcoholic fatty liver disease, liver inflammation, and any condition that could affect liver function would be a reason to avoid alcohol,” notes Favini.
- Corticosteroids are one example, as are TNF inhibitors for inflammation and chemotherapy for cancer.
- They produce immune molecules called antibodies or immunoglobulins that they can either display on their surface or secrete.
Additionally, the role of alcohol-induced changes in the microbiome on immunity should be studied. Recent studies have shown that the microbiome modulates immunity in the gut, and in turn, immunity modulates the microbiome in the gut (Belkaid and Hand 2014). Only two studies have examined alcohol-induced changes in colonic (Mutlu, Gillevet et al. 2012) and fecal microbiomes (Chen, Yang et al. 2011), and both studies focused on individuals with AUD.
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Some research even suggests that a few libations — 1 drink a day for women and 2 a day for men — may even boost the immune system. Fatty liver is usually completely reversible in about four to six weeks if you completely abstain from drinking alcohol. Cirrhosis, on the other hand, does alcohol weaken your immune system is irreversible and likely to lead to liver failure despite abstinence from alcohol, according to Dr. Menon. But when you’ve ingested too much alcohol for your liver to process in a timely manner, the toxic substance begins to take its toll on your body, starting with your liver.
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). Elevated levels of ROS cause oxidative stress which has been shown to play a role in several harmful processes including cancer development, atherosclerosis, diabetes, and inflammation (Tuma and Casey 2003). And it’s not just that you’re more likely to get a cold — excessive drinking is linked to pneumonia and other pulmonary diseases.
Alcohol and the Innate Humoral Response to Infections
Few studies have investigated the effects of alcohol abuse on complement activation and its relationship with the incidence and severity of infection; instead, the focus of studies on alcohol-induced alterations in complement has been on liver injury (Pritchard et al. 2008). However, alcoholic patients frequently have abnormally low levels of complement in the blood. In addition, animal studies have indicated that acute alcohol intoxication can decrease complement activation in response to tissue injury resulting from disruptions in blood supply (i.e., ischemic injury). In contrast, chronic alcohol intake can activate the complement response (Roychowdhury et al. 2009), both by inducing the biochemical pathways that lead to activation of the complement cascade and by suppressing processes to terminate or regulate the cascade (Bykov et al. 2007).