Bagby and colleagues review substantial evidence that alcohol further disrupts the immune system, significantly increasing the likelihood of HIV transmission and progression. 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. Although the innate immune response is immediate, it is not specific to any given pathogen.
- Response to different stressors is mediated by several neural circuits that converge on the paraventricular nucleus (PVN) of the hypothalamus (Myers, McKlveen et al. 2014).
- As is the case with other organs, alcohol’s specific effects on the conducting airways depend on the route, dose, and length of the exposure (Sisson 2007).
- Finally, an emerging informatics approach that can piece together these extensive data sets and build a network between the immune response elements, the HPA axis, and the time-course/dose response of ethanol while emphasizing in vivo studies from rodent, non human primate, and humans is urgently required.
- Also, bacteria that escape this area can change the immune system in your liver, which can lead to inflammation and, potentially, alcoholic liver disease.
- 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).
- Upon phosphorylation, HSP90 increases its association with endothelial nitric oxide synthase (eNOS) in cilia, which then activates the cyclase–kinase cascade, resulting in increased CBF (Simet et al. 2013b).
- The course and resolution of both bacterial and viral infections is severely impaired in alcohol-abusing patients, resulting in greater patient morbidity and mortality.
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. Because alcoholics are at increased risk for hepatitis B (HepB) infections, immunization with a HepB vaccine is recommended. Another study (Rosman et al. 1997) demonstrated that the impaired antibody response in alcoholic patients (i.e., with consumption levels of 230 ± 16 g/day ethanol for 26.4 ± 1.8 years) can be improved by doubling the dose of HepB vaccine from 10 μg to 20 μg at 0, 1, and 6 months.
Cellular Responses
In contrast to these observations, moderate consumption of beer (330mL for women and 660mL for men) for 30 days resulted in a significant increase in the number of leukocytes, mature CD3+ T lymphocytes, neutrophils and basophils in women, while only basophils were increased in men (Romeo, Warnberg et al. 2007). “Alcohol has diverse adverse effects throughout the body, including on all cells of the immune system, that lead to increased risk of serious infections,” said Dr. E. Jennifer Edelman, a Yale Medicine addiction medicine specialist. 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 heart disease, liver disease, and increased risk of cancer. 1T-cell activation was assessed by measuring the expression of human leukocyte antigen (HLA)-DR on the patient’s CD8 cells.
- A high alcohol intake, whether long-standing excessive alcohol consumption or binge drinking, has been shown to nearly double the risk of acute respiratory distress syndrome, a complication of COVID-19 that makes breathing difficult.
- 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.
- For men, the CDC defines excessive alcohol consumption as five or more drinks on one occasion or 15 or more drinks per week.
- It constitutes the first line of defense against molecules, which are either pathogen-derived or a danger signal themselves, and not seldom both.
- 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).
This is because studies suggest that heavy drinking — defined as over 8 drinks per week for women and 15 per week for men — can disrupt key immune pathways, make people more susceptible to infection, and weaken the immune system. Catalase is localized to peroxisomes and requires hydrogen peroxide to oxidize alcohol into water and acetaldehyde. Alcohol metabolism can also take place in the pancreas by acinar and pancreatic stellate cells, which contributes to the development of alcoholic pancreatitis (Vonlaufen, Wilson et al. 2007).
Long-term effects of alcohol on the immune system
Alcohol exposure, and particularly chronic heavy drinking, affects all components of the adaptive immune system. Studies both in humans and in animal models determined that chronic alcohol abuse reduces the number of peripheral T cells, disrupts the balance between different T-cell types, influences T-cell activation, impairs T-cell functioning, and promotes T-cell apoptosis. Chronic alcohol exposure also seems to cause loss of peripheral B cells, while simultaneously inducing increased production of immunoglobulins.
In healthy individuals, the bone marrow produces approximately 120 billion neutrophils per day (Cartwright et al. 1964; von Vietinghoff and Ley 2008). Moreover, bone-marrow neutrophil production is significantly increased 24 to 48 hours after a systemic bacterial infection (Melvan et al. 2011). Alcohol exposure suppresses neutrophil does alcohol weaken your immune system production by the bone marrow and other blood cell–producing (i.e., hematopoietic) tissues (Melvan et al. 2011; Raasch et al. 2010; Siggins et al. 2011). This decreased neutrophil proliferation may account for the decreased number of neutrophils found in the lungs during the host response to pneumonia following alcohol consumption.
1. Cellular Responses—Phagocytosis and Oxidative Burst
Thus, alcohol interferes with various processes necessary to deliver neutrophils to the site of an infection, such as expression of a molecule called CD18 on PMNs in response to inflammatory stimuli and PMN “hyperadherence” to endothelial cells following appropriate stimulation (MacGregor et al. 1988). 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. B cells are responsible for the second arm of the immune response (i.e., the humoral immunity) that is mediated not by specific cells but by immune molecules (i.e., antibodies) produced and secreted by B cells in response to exposure to a pathogen. There are different types of Igs (e.g., IgA, IgM, and IgG) that all have specific functions during the immune response. Thus, although the total number of circulating B cells does not differ significantly between people with and without AUD, people with AUD have elevated levels of circulating IgA, IgM, and IgG (Spinozzi et al. 1992).