Sober living
5 JULY 2021
Those studies showed decreased cytolytic activity of NK cells in C57BL/6 mice consuming 20 percent ethanol for 4 weeks; however, no differences existed in the metastasis of B16-BL6 melanoma cells in alcohol-consuming and control animals (Meadows et al. 1993). The presence of ethanol in an in vitro culture of spleen cells also suppressed NK cell cytotoxic activity against MADB106 tumor cells (Yirmiya et al. 1992). Heavy drinking and chronic alcohol use can significantly impact the immune system and decrease immune function. Beside the immune cells-mediated host defense, mucous epithelial cells provide a physical barrier and contribute to regulation of innate and as well adaptive immunity. In the last years, microbiota has been extensively studied regarding its impact on various diseases. There is also evidence that alcohol abuse disrupts those epithelial barriers in gastrointestinal and respiratory tracts.
The activated T cells multiply and begin secreting cytokines, which, in turn, activate cytotoxic T cells that can then recognize, bind to, and destroy cells infected by the invading bacteria. And high fat diets over time can upset the balance of bacteria in your gut that can help immune response. Look for low-fat dairy with no added sugar, along with lean protein like seafood, turkey, and chicken, or lean cuts of beef with any visible fat cut off. Also, being obese seems to make you more likely to get the flu and other infections, like pneumonia. These foods may help your body make more of the white blood cells you need to fight off infections. Fresh produce and nuts and seeds pack a lot of zinc, beta-carotene, vitamins A, C, and E, and other nutrients you need for a healthy body.
Alcohol-mediated effects on CD8+ T-cell function also have been linked to impaired immunity in the lung in response to influenza infection (Meyerholz et al. 2008). Whether the increased viral load measured in SIV-infected chronic alcohol-fed macaques can be attributed to diminished CD8+ T-cell function remains to be established (Bagby et al. 2006; Kumar et al. 2005). Both the innate and the adaptive immune response are critical for effective host defense to infectious challenges. Multiple aspects of both arms of the immunity response are significantly affected by alcohol abuse, as described in the following sections.
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. In addition, most studies have been done in vitro using primary cells or cell lines in the presence of rather high, constant doses of ethanol. Similarly, most rodent studies to date have focused on acute/short-term binge models utilizing high concentration of ethanol (20% ethanol) as the sole source of fluid, a possible stressor in itself.
The molecular mechanisms underlying ethanol’s impact on the adaptive immune system remain poorly understood. Cytokines are affected by alcohol on several levels as they are induced by certain pathways affected by alcohol, which again, in turn, can be modulated by other cytokines. Summarized, this makes it difficult to differentiate between altered cytokine actions and altered cytokine release. does alcohol suppress immune system In an in vitro model of acute inflammation, pretreatment of human lung epithelial cells with alcohol (85 or 170 mM) for 24 or 72 hours reduces IL-8 release upon their stimulation with IL-6. In contrast to the treatment of cells prior to inflammatory stimulation, treating cells with alcohol afterward reduces the IL-8 release significantly after an incubation period of one hour.
These disruptions to the composition of the gut microbiota and to gut barrier function have important implications beyond the intestinal system. For example, Nagy discusses how the leakage of bacterial products from the gut activate the innate immune system in the liver, triggering inflammation that underlies ALD, a condition that affects more than 2 million Americans and which eventually may lead to liver cirrhosis and liver cancer. Infection with viral hepatitis accelerates the progression of ALD, and end-stage liver disease from viral hepatitis, together with ALD, is the main reason for liver transplantations in the United States. The article by Dolganiuc in this issue explores the synergistic effects of alcohol and hepatitis viruses on the progression of liver disease as well as alcohol consumption’s injurious effect on liver antiviral immunity. Mandrekar and Ju contribute an article that homes in on the role of macrophages in ALD development, including recent insights into the origin, heterogeneity, and plasticity of macrophages in liver disease and the signaling mediators involved in their activation and accumulation.
For example, alcohol inhibits the functions of the cells that ingest and destroy invading microorganisms (i.e., neutrophils, monocytes, and macrophages). Both acute and chronic alcohol exposure also alter the production of signaling molecules that help coordinate the immune response (i.e., cytokines). Finally, alcohol adversely affects the functions of the cells that mediate the immune response against specific microorganisms and long-term immunity (i.e., T cells and B cells). As a result, alcoholics have an increased susceptibility to diseases caused by bacterial infections, such as tuberculosis and pneumonia. Alcoholics also may be more susceptible to infections from the virus that causes AIDS. In addition, alcohol intoxication can exacerbate the immune suppression that occurs after traumatic injuries.
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