Does gliadin induce an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3?
Gliadin binds to CXCR3 and leads to MyD88-dependent zonulin release and increased intestinal permeability.
A stromelysin increase, localized primarily to the juxtacanalicular region of the meshwork, the putative site of the aqueous humor outflow resistance, should degrade trabecular proteoglycans, the putative outflow resistance source, and allow their uptake and further degradation by the juxtacanalicular cells. If diminished juxtacanalicular extracellular matrix turnover is responsible for the glaucomatous reduction in aqueous humor outflow, an increase in stromelysin in this specific area of the meshwork should ameliorate the problem. Thus, the observations support the working hypothesis and may explain the efficacy of this treatment for glaucoma.