The levels of CCL26 in the serum and in brain tissues as well as the protein expression of CCR3 in brain tissues were positively correlated with the inflammatory scores of brain tissues from EAE rats and were negatively correlated with the protein expression of claudin-5.
In EAE-affected mice, OPCs were mostly associated with microvessels that showed altered claudin-5 and occludin tight junction (TJ) staining patterns and barrier leakage.
Administration of a P2X7R antagonist to the immunized rats significantly reduced clinical signs of EAE and enhances protein expression of both claudin-5 and PDGFβR.