Similarly, vitamin C, also an antioxidant, is important for phagocytic activity of neutrophils and monocytes, and enhances T cell responses (Strohle and Hahn 2009). Thiamine, also known as vitamin B1, contributes to the activation of T cells, suppresses oxidative stress-induced NFκB activation in macrophages, and serves as an anti-inflammatory factor (Manzetti, Zhang et al. 2014). Antigen-specific responses are decreased in folate-deficient humans and animals (Dhur, Galan et al. 1991). T and B cell activation in the presence of retinoic acid results in the up-regulation of gut-homing molecules and generation of IgA-secreting B cells (Mora, Iwata et al. 2008). Consequently, deficiency in vitamin A results in the impairment of mucosal responses (Mora, Iwata et al. 2008). Vitamin D has long been known to have a critical role in calcium and phosphorous homeostasis.

The microbiome is the bacteria that naturally live on our skin, in our digestive tract and in part of the reproductive system in females. These bacteria are necessary for optimal health, and their presence helps prevent harmful bacteria from having the space needed to grow. 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. In the lungs, for example, alcohol damages the immune cells and fine hairs that have the important job of clearing pathogens out of our airway. The spike in alcohol sales has alarmed health experts and officials around the world, who are concerned that increased drinking could make people even more vulnerable to the respiratory disease.

How much alcohol does it take to weaken your immune system?

The rest of the SCFAs reach the circulatory system via the superior or inferior mesenteric vein, reaching the brain and crossing the blood–brain barrier thanks to monocarboxylate transporters thus being able to act as signaling molecules between the gut and the brain [74]. Specifically, chronic alcohol consumption could reduce the SCFAs count through the reduction in some Firmicutes genera, such as Faecalibacterium and Ruminococcaceae, on which the production of SCFAs depends [75,76]. Furthermore, it has been described that alcohol consumption would also have effects on other microbiota derived metabolites, leading to increases in branched-chain amino acids [77] and peptidoglycans [78]. However, studies showing the effect of alcohol on these microbiota derived metabolites are scarce.

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 does alcohol weaken your immune system effects. Suppression of inflammatory factors like cytokines is further achieved by the inhibition of histone deacetylases (HDACs) activity. Finally, SCFAs have been shown to modulate immune inflammation responses in extraintestinal organs such as the brain, by acting on microglia and astrocytes. In addition, production of IL-10 in response to TLR2/6 stimulation was increased (Pruett, Zheng et al. 2004).

Drinking impairs immune cells in key organs

For example, alcohol alters the numbers and relative abundances of microbes in the gut microbiome (see the article by Engen and colleagues), an extensive community of microorganisms in the intestine that aid in normal gut function. Alcohol disrupts communication between these organisms and the intestinal immune system. Alcohol consumption also damages epithelial cells, T cells, and neutrophils in the GI system, disrupting gut barrier function and facilitating leakage of microbes into the circulation (see the article by Hammer and colleagues). Interestingly, in addition to supporting neuroinflammation, TLR signaling is likely engaged in the mechanisms of regulation of the functional activity of neurotransmitter systems, which may contribute to the formation of a pathological demand for alcohol [106]. Together with TLRs activation, the production of cytokines, which can cross the blood–brain barrier (BBB), have harmful effects at CNS level [102].