Alcohol or ethanol is one of the most abused substances, and is one of the leading causes of premature death, globally. Owing to its complexity and direct contact with ingested alcohol, the intestine is the primary source of alcohol-associated pathologies. The gut is the largest reservoir of bacteria in the body, and physiologically, maintains a barrier preventing bacteria from translocating out of the intestinal lumen. However, this intestinal barrier gets compromised following alcohol exposure, causing life-threatening systemic complications including sepsis and multiple organ failure. 

Alcohol is a main confounding factor in pathology related to trauma. Researches from both human and animal studies showed that alcohol disturbs the intestinal barrier and its function, which is precipitated by a “second hit” from traumatic injury. Disruptions in either the intestinal mucus or epithelial barrier can cause pathogenic bacterial translocation. This can cause systemic infections, sepsis, and multiple organ failure, which emphasizes the significance of maintaining barrier integrity. It has been observed that alcohol consumption can cause disturbances in all components of the intestinal barrier, which further causes an increase in bacterial translocation and infection.

The mucus layer and its alteration by alcohol exposure acts the first line of defense against pathogenic organisms within the intestinal lumen. Researchers suggest that prolonged alcohol exposure results in increased mucin production and several components of the mucin biochemical composition get altered following prolonged alcohol exposure. In addition, alcohol also disrupt the integrity of tight junction complexes between intestinal epithelial cells.

Furthermore, alcohol intoxication poses its effects on neutrophil infiltration, which increases into different organs, including the lungs and intestines. Although the role of neutrophils is unclear in disease models, numerous studies have found that, the inflammatory microenvironment following alcohol exposure may allow neutrophils to aggravate tissue damage in numerous organs including intestine.

Besides neutrophil activity, alcohol has significant effect on immune cells at sites outside the intestine, including in the spleen, thymus, and on circulating lymphocytes. Intestinal studies suggest that alcohol may have inflammatory effects, which further compromise the intestine’s ability to prevent bacteria from passing into the body. Studies from the laboratory also show a decrease in Th1 cells, particularly in mesenteric lymph nodes (MLNs), along with decreases in IL-12 following alcohol intoxication. Reduced Th1 effector cells present following alcohol intoxication and burn injury may allow bacteria and other pathogens to progress across the intestinal barrier.

Thus, several studies have studied the effects of alcohol exposure on the microbiome within the intestines. A recent study determined the effects of chronic daily alcohol consumption and revealed that dysbiosis, a microbial imbalance, in experimental animals after 10 weeks. Few studies have found an association between microbial dysbiosis to alcoholic liver disease and showed that administration of probiotics can aid in decreasing hepatic inflammation. The present study also showed evidence that combined alcohol intoxication followed by traumatic burn injury lead to a significant increase in bacterial translocation across the intestinal barrier.

Source: Hammer AM, Morris NL, Earley ZM, Choudhry MA. The First Line of Defense: The Effects of Alcohol on Post-Burn Intestinal Barrier, Immune Cells, and Microbiome. Alcohol Res. 2015;37(2):209-222.