As a result, bacteria may leak from the GI tract into your bloodstream, which can itself make you sick. Also, bacteria that escape this area can change the immune system in your liver, which can lead to inflammation and, potentially, alcoholic liver disease. “By damaging those cells in your intestines, it can make it easier for pathogens to cross into your bloodstream,” says Nate Favini, MD, medical lead at Forward, a preventive primary care practice. 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. In addition to decreasing the antimycobacterial activity of macrophages, alcohol consumption also reduces macrophage response to immune system modifiers.
In rats that received alcohol infusions for 1, 3, or 5 hours, for example, the Kupffer cells in the liver produced and secreted increased levels of superoxide anions, whether or not the cells were activated by contact with pathogens. Together, these observations imply that alcohol may have a dual negative effect on the body’s oxygen-radical production. First, alcohol may inhibit oxygen-radical and nitric oxide production in macrophages in the lung, where these substances are essential for killing microorganisms.
Effects of alcohol on adaptive immunity
Alcohol-induced changes in tight junctions cause increased intestinal leaks that lead to translocation of bacteria-derived products such as lipopolysaccharide (LPS). These molecules enter the circulation to the liver where they activate endothelial and stellate cells as well as hepatocytes, resulting in a chronic inflammatory environment aggravating organ injury. Both the innate and the adaptive immune response are critical for effective host defense to infectious challenges.
- Similarly, vitamin C, also an antioxidant, is important for phagocytic activity of neutrophils and monocytes, and enhances T cell responses (Strohle and Hahn 2009).
- This alcohol-mediated dendritic cell dysfunction prevents the organism from generating virus-specific adaptive immune responses involving CD4+ and CD8+ lymphocytes, which may contribute to the acquisition and persistence of hepatitis C infection (Siu et al. 2009).
- But the investigators were surprised to find that the monkeys deemed as moderate drinkers demonstrated an enhanced vaccine response.
- IL-2 is one of the most important T-cell–produced cytokines; it promotes the proliferation and survival of certain T-cell subpopulations.
- 3The HIV (or SIV) set point is the stable viral load that is established in an HIV-infected person after the initial phase of the infection, when the person’s immune systems tries to fight the virus.
Studies in rhesus macaques have helped elucidate the effects of alcohol on DC development in hematopoietic tissues and the functional activities of the DCs (Siggins et al. 2009). In these studies, chronic alcohol exposure decreased the pools of myeloid DCs in the bone marrow and peripheral blood. Alcohol also suppressed expression of the co-stimulatory molecule CD83 during DC maturation, which may attenuate the ability of DCs to initiate T-cell expansion (Siggins et al. 2009). The complexity of the innate and adaptive immune responses are increased further by the fact that different subsets of immune cells may reside in specific organs, such as the liver, lungs, brain, skin, bones, or muscles. This complex structure of the immune system with its multitude of different cells with diverse functions allows the organism to defend itself properly against the hugely diverse pathogens it may encounter, without endangering its own cells.
Overview of the Human Immune System
Finally, reduced T-cell proliferation may be attributed to the increased production of immunoregulatory cytokines (e.g., IL-10 and TGF-β) caused by alcohol. The initial inflammatory response to pathogens normally is turned off by regulatory cytokines whose production typically is induced in a later phase of the infection. The most studied immunoregulatory cytokines are IL-10 and transforming growth factor beta (TGF-β), both of which are produced by macrophages and T cells. IL-10 promotes humoral immunity and inhibits cell-mediated immunity by reducing the production of several cytokines, including inflammatory cytokines, and by preventing the multiplication (i.e., proliferation) of T cells. Acute alcohol exposure increases IL-10 production in cultured human monocytes both in the absence and presence of stimulation by bacterial antigens and thus may interfere with the normal interaction of the cell-mediated and humoral immunities. In chronic alcohol abusers, particularly those with alcoholic liver disease, the levels of TNF-α, IL-1, and IL-6 in the blood are significantly elevated.
Chronic as well as acute alcohol consumption also reduces the ability of phagocytes to ingest and break down pathogenic bacteria. For example, cultured human monocytes exposed to alcohol showed reduced phagocytic functions; moreover, the cells produced less of a receptor protein that is required for the ingestion of antibody-coated particles. In mice, both short-term and long-term alcohol feeding reduced the phagocytic ability of macrophages residing in the membrane lining the abdominal cavity.
Effects on CD8+ (Cytotoxic) T-Cells
These cells act as phagocytes—that is, they engulf pathogens and ingest them in a process called phagocytosis. In addition, they can excrete toxic substances from their granules that can kill pathogens. PMNs produce a host of bacteria-killing (i.e., bactericidal) molecules (e.g., myeloperoxidase, defensins, azurophil-derived bactericidal factors, bactericidal does alcohol suppress your immune system permeability-increasing protein, cationic proteins, gelatinase, and lactoferrin). In addition, PMNs participate in the regulation of the local defense response by releasing signaling molecules called cytokines and chemokines (e.g., tumor necrosis factor [TNF]-α; interleukin [IL]-1β, IL-6, and IL-8; and macrophage inflammatory protein [MIP]-2).
However, all immunoglobulins produced by one B-cell and its daughter cells specifically recognize the same antigen. Alcohol feeding suppresses the production and secretion of certain acute-phase proteins (i.e., type II cell surfactant). This effect may contribute to lung injury in response https://ecosoberhouse.com/ to inflammation (Holguin et al. 1998). Fatty liver, early stage alcoholic liver disease, develops in about 90% of people who drink more than one and a half to two ounces of alcohol per day. So, if you drink that much or more on most days of the week, you probably have fatty liver.
Impoverished alcoholics thus are prone to reactivation of TB, and if their medication use is erratic, a strain of M. Alcohol can have a range of harmful effects on the body, which can diminish a person’s immune response and put them more at risk for COVID-19. Past research shows alcohol consumption leads to more severe lung diseases, like adult respiratory distress syndrome (ARDS) and other pulmonary diseases, including pneumonia, tuberculosis, and respiratory syncytial virus.