Gut-Liver Axis
Excessive alcohol consumption results in GI tract dysfunction including disruption of the intestinal barrier and exposure of the liver to microbes and gut-derived pathogen-associated molecular patterns (PAMPs). The upper GI tract is exposed to the highest amount of alcohol but little is known about the impact of alcohol on GI tract inflammation. This study aims to gain insight into the early effects of alcohol binges on GI inflammation.
Alcohol binges induced a proximal small intestine (PSI) enteropathy with neutrophil recruitment, neutrophil extracellular traps (NETs), and increased serum endotoxin. Neutrophil recruitment and serum endotoxin normalized 24 hours after the last binge with persistent PSI villous blunting. While alcohol generated ROS, administration of the anti-oxidant, NAC, failed to prevent the PSI enteropathy, neutrophil recruitment, or disruption of the intestinal barrier. We found robust upregulation of Gal-3 and CXCL10 in the PSI after alcohol binges that likely mediate neutrophil recruitment and activation.
Conclusion: Alcohol binges result in a PSI enteropathy, transient infiltration of neutrophils, and NETs. While neutrophils are recruited to the GI tract to produce NETs in response to alcohol, this phenomenon is independent of ROS production.
