NF-κB-coupled IL17 mediates inflammatory signaling and intestinal inflammation in Artemia sinica

Nuclear factor-kappa B (NF-kappa B) plays a role as a rheostatic transcription factor in regulating intestinal inflammation, and its disruption or constitutive activation leads to inflammation and injury. However, the molecular mechanisms of NF-kappa B regulation remain largely unknown. In this study, the NF-kappa B-regulated host defenses against pathogen infections and facilitation of IL17 expression during stimulation with different bacteria were investigated. Intestinal inflammation was induced by dextran sulfate sodium, and NF-kappa B activity was inhibited in an intestinal injury model. Mannose receptor C type, ABF1/2, serpin B13, lysozyme, and beta-arrestin were significantly controlled by NF-kappa B in the inflamed intestinal tissue. High levels of NF-kappa B activation resulted in less pervasive intestinal damage and the maintenance of intestinal barrier integrity. Intestinal injury robustly increased the expression of IL17. NF-kappa B activation was enhanced by IL17 deficiency in the intestinal injury model. IL17 inhibition aggravated intestinal inflammation, leading to loss of epithelial architecture and the infiltration of inflammatory cells. These data suggest that NF-kappa B and IL17 play key mediator roles in the maintenance of gut epithelial integrity and immune homeostasis.

Automated summary

Nuclear factor-kappa B (NF-kappa B) plays a crucial role in regulating intestinal inflammation and maintaining gut epithelial integrity. Its activation controls the expression of various factors and helps to reduce intestinal damage. IL17, on the other hand, enhances NF-kappa B activation and contributes to intestinal inflammation.