The effect of pro-inflammatory cytokines on the transport of taurocholic acid (TCA) in a cell-based intestinal model

In the modern world, one of the diseases that is spreading at an alarming rate is inflammatory bowel disease (IBD). When it comes to inflammatory bowel disease (IBD), bile acid malabsorption (BAM) is a prevalent but frequently disregarded symptom. The absorption and transfer of fats, minerals, and vitamins depend on bile acids, which are synthesized from cholesterol. The ileum, the last section of the small intestine, is where bile acids are reabsorbed and sent back to the liver in amounts of about 95%. This enterohepatic cycle is referred to as enterohepatic cycle. Bile acid malabsorption is brought on by the disruption of this cycle. In this study, we studied the influence of tumor necrosis factor (TNF- α) in a model bile acid. TNF- α is a pro inflammatory cytokine. Upon the exposure of TNF- α in the model bile acid, it can cause adverse effects in the intestine. Using an in vitro model based on Caco-2 cell layers cultured in transwells, this study investigated the effects of TNF- exposure on the intestinal absorption of conjugated bile acids. Our research demonstrates that after 48 hours of exposure to Caco-2 cells up to 800 pg/mL TNF, a realistic intestinal TNF- α concentration, the transit rate of taurocholic acid (TCA) is reduced. Additionally, the intestinal Caco-2 cell layers' ability to transport bile acids in a physiologically significant combination was reduced after the cells were exposed to TNF- α. According to the combined data, TNF-α inhibits intestinal bile acid reabsorption by decreasing the expression of bile acid transporters, which affects bile acid intestinal kinetics and causes bile acid malabsorption in the intestine. Our study presents new perspectives on the implications of TNF- α exposure.