IL-6 levels after exposure to lipopolysaccharide through injection or alcohol consumption
Alcohol interacts with the immune system in multiple ways that are not fully understood but which likely contribute to alcoholic pathologies and may be relevant to the study and treatment of alcohol dependence. Alcohol consumption permeabilizes the gut, allowing the release of lipopolysaccharide (LPS), an endotoxin that elicits the production of pro-inflammatory cytokines (protein signaling molecules produced by immune cells) including interleukin-6 (IL- 6). As excessive inflammation may lead to shock, there exists a protective mechanism, endotoxin tolerance, that suppresses the inflammatory response to LPS after an initial exposure. Because of the phenomenon of endotoxin tolerance, we hypothesized that chronic alcohol exposure would result in the suppression of the IL-6 response to LPS. In this study, mice were treated with a single injection of LPS, repeated injections of LPS, or one injection of LPS after a period of chronic alcohol dinking, and then the levels of IL- 6 were measured in order to assess the immune response. It was found that while mice given a single injection of LPS showed a significant increase in IL-6, those given repeated injections of LPS did not show any increase; they had developed tolerance to the multiple exposures of LPS. After 18 days of chronic voluntary intake of alcohol, the IL-6 response to LPS was also suppressed. This shows that chronic alcohol consumption produces an alteration in the immune system that could play a possible role in the development of alcohol dependence. Further research is necessary to determine if this area of study could lead to the better understanding and treatment of alcohol dependence.