Abstract: Clostridium difficile infection has been shown to cause a defective intestinal epithelial tight junction barrier. IL-1β, IL-6, and TNF-α are hypothesized to be the main players in the development of intestinal inflammation and cause an increase in intestinal tight junction permeability. This study showed that cytokines had different effects on tight junction disruption based on either low or high concentration. Both C. difficile toxins were able to disrupt tight junctions, although TcdB had a greater effect overall. We also tested the toxins' ability to induce NF-kB activation, and based on the results, TcdB was more potent than TcdA in inducing NF-kB.Summary: C. difficile infection has been shown to cause a defective intestinal epithelial tight junction barrier. IL-1β, IL-6, and TNF-α are hypothesized to be the main players in the development of intestinal inflammation and cause an increase in tight junction permeability. This study aims to show the effects of those cytokines and toxins on tight junction barrier over time.
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