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Microbiota produces neurotransmitters, tryptophan metabolites, fermentation metabolic by-products such as short-chain fatty acids (SCFAs), the release of cytokines by immune cells and gut hormone signaling. Some of these molecules can activate the vagus nerve or reach the brain and liver via systemic circulation. Alcohol consumption causes dysregulation in the intestinal microbiota, which leads to an alteration in this communication and subsequently causes alterations in brain and liver functions. Clinicians have long observed an association between excessive alcohol consumption and adverse immune-related health effects such as susceptibility to pneumonia. Several lines of evidence show that the number and function of B-cells are reduced by chronic alcohol. For example, chronic alcoholics exhibit loss of B-cells in the periphery and a reduced capacity to generate protective antibodies (Cook et al. 1996).

Additional studies in rodents assessed the effects of alcohol on the effectiveness of bacillus Calmette-Guérin (BCG) vaccination, which protects against tuberculosis. The studies found that when animals consumed ethanol before BCG vaccination, they were not protected against a subsequent pulmonary challenge with M. In contrast, mice that consumed ethanol after the BCG vaccination were protected against a subsequent M. Taken together, these data suggest that chronic ethanol exposure interferes with immunity does alcohol suppress immune system to new antigens but not with immunity established before alcohol consumption. Chronic alcohol consumption reduces B-cell numbers, decreases antigen-specific antibody responses, increases the production of auto-antibodies, and interferes with B-cell development and maturation. Although most research has focused on the effects of heavy alcohol consumption on the immune system, several studies have also confirmed that even moderate consumption can have significant effects on the immune system.

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T cells expressing the CD8 T cell co-receptor are known as cytotoxic T cells and eliminate host cells infected with intracellular pathogens as well as tumor cells. B cells mature into plasma cells that produce antibodies, also known as immunoglobulins (Ig), to eliminate extracellular microorganisms and prevent the spread of infection. The adaptive immune response can be distinguished from innate immunity by the capability of generating immunological memory, or protective immunity against recurring disease caused by the same pathogen (Janeway 2008). Alcohol consumption increases intestinal permeability through the suppression of intestinal tight junction protein expression. This alteration allows the translocation of bacterial products to the systemic circulation. The gut-derived bacterial components together with LPS activate the immune cells localized in the systemic circulation or in target organs such as liver and brain.

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. 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. The innate immunity has evolved during millions of years, and thus, equivalent or comparable components are found in most vertebrates, invertebrates, and even plants. It constitutes the first line of defense against molecules, which are either pathogen-derived or a danger signal themselves, and not seldom both.

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(B) The gut microbiota is in close interaction with both the innate and the adaptive immune system. This interaction is frequently driven by SCFAs, which modulate local as well as systemic immune response. SCFAs can bind to G-protein-coupled receptors as FFAR2 and FFAR3 present on the surface of gut epithelial cells and immune cells including dendritic cells, macrophages and neutrophils, and are therefore important regulators of inflammatory response. SCFAs also promote the activation of B cells and the development of Treg CD4+T cells—for example, increasing secretion of IL-10 with important anti-inflammatory effects.

By illuminating the key events and mechanisms of alcohol-induced immune activation or suppression, research is yielding deeper insights into alcohol’s highly variable and sometimes paradoxical influences on immune function. The insights summarized in this issue of ARCR present researchers and clinicians with opportunities to devise new interventions or refine existing ones to target the immune system and better manage alcohol-related diseases. The white blood cells, tissues and organs that make up our body’s immune system are designed to fight off infections, disease and toxins. 4Expression of TNF-α and IL-1β requires the actions of a protein called nuclear factor (NF)- B. 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).

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5IgA is an antibody that plays a critical role in immune responses in the mucous membranes. These membranes line the body cavities exposed to the external environment (e.g., the GI tract, respiratory tract, nostrils, mouth, or eyelids) and therefore are likely to come in contact with outside pathogens. These may include infections after surgery, traumatic injury, or burns; accelerated progression of HIV disease; adult respiratory distress syndrome and other opportunistic lung infections; and infection with hepatitis C virus, cirrhosis, or liver cancer (hepatocellular carcinoma).

alcohol lowers immune system

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