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 particular, the levels of antibodies against liver-specific autoantigens are increased in patients with alcoholic liver disease and may promote alcohol-related liver damage.

Abstinence partially restored antibody responses against hepatitis antigens in a mouse model (Encke and Wands 2000). Alcohol consumption also influences T-cell activation both in humans and in mouse models (Cook et al. 1991, 1995). Thus, C57BL/6 or BALB/c mice that consumed 20 percent ethanol in water for up to 6 months showed a greater frequency of activated T cells, increased rapid IFN-γ response, and heightened sensitivity to low levels of TCR stimulation, with no requirement for a second signal (Song et al. 2002; Zhang and Meadows 2005). The effects of chronic alcohol exposure are not limited to phenotypic changes in T cells but also include T-cell functions. Among other reactions, LPS injection normally triggers lymphocyte migration out of the circulation and into tissues and the lymphatic system (Percival and Sims 2000).

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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). Alcohol feeding suppresses the production and secretion of certain acute-phase proteins does alcohol weaken your immune system (i.e., type II cell surfactant). This effect may contribute to lung injury in response to inflammation (Holguin et al. 1998). Healthy habits, such as being active, eating a balanced diet, and getting enough sleep, can keep your immune system strong.

Some B-cells, however, become memory cells that will remain dormant in the body for years and can be activated rapidly if a second infection with the same pathogen occurs. The activities of T-cells and B-cells are intricately intertwined through the actions of various cytokines to orchestrate an effective immune response to any pathogen the organism may encounter. Molecular mechanisms of the dose-dependent effects of alcohol on the immune system and HPA regulation remain poorly understood due to a lack of systematic studies that examine the effect of multiple doses and different time courses. There may be important differences in the effects of ethanol on the immune system depending on whether the study is conducted in vitro or in vivo, as the latter allows for a complex psychogenic component in which stress-related hormones and immune-signaling molecules interact.

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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. The innate cellular response, which is mediated primarily by monocytes/macrophages and neutrophils, involves the recognition, phagocytosis, and destruction of pathogens—processes essential to subsequent adaptive responses. Acute and chronic alcohol abuse can interfere with the actions of these cells at various levels. 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.

Similarly, consumption of 10% (w/v) ethanol in tap water ad libitum for 2 days in mice resulted in decreased bone marrow DC generation, decreased expression of CD80 and CD86, impaired induction of T cell proliferation, and a decrease in IL-12 production (Lau, Abe et al. 2006). In addition to reducing T-cell numbers, chronic alcohol exposure disrupts the balance between different T-cell types (i.e., T-cell homeostasis), leading to a shift toward a memory phenotype. Specifically, people who had consumed 30.9 ± 18.7 alcoholic drinks/day for approximately 25.6 ± 11.5 years exhibited a decreased frequency of naïve (i.e., CD45RA+) CD4 and CD8 T cells, as well as an increased frequency of memory T cells (i.e., CD45RO+) (Cook et al. 1994). Another study conducted in humans with self-reported average alcohol consumption of approximately 400 g/day also found an increase in the percentage of both CD45RO+ memory CD4 cells and CD8 cells (Cook et al. 1995). Thus, studies in C57BL/6 mice demonstrated that chronic ethanol consumption (20 percent ethanol in water for up to 6 months) decreased the frequency of naïve T cells and increased the percentage of memory T cells (Song et al. 2002; Zhang and Meadows 2005). This loss of naïve T cells could result from decreased T-cell production in the thymus; increased cell death (i.e., apoptosis) of naïve T cells; or increased homeostatic proliferation.