CCL26 and CCR3 are associated with the acute inflammatory response in the CNS in experimental autoimmune encephalomyelitis.

Chemokine ligand 26 (CCL26) is a member of the eotaxin family. It works by interacting exclusively with chemokine receptor 3 (CCR3) and acts as an eosinophil-selective chemoattractant. There is an emerging role for eotaxins in autoimmune diseases. Studies have reported that chemokine ligand 11 (CCL11) and CCL26 are upregulated in patients with neuromyelitis optica spectrum disorder (NMOSD) during remission, CCL26 levels appear to be decreased in relapsing-remitting multiple sclerosis (RRMS), whereas CCL26 levels are significantly increased in secondary progressive multiple sclerosis (SPMS), indicating that CCL26 participates in the pathogenesis of multiple sclerosis (MS). We investigated the levels of CCL26, CCR3 and claudin-5 (a marker of changes in BBB (blood-brain barrier) permeability) at different stages of experimental autoimmune encephalomyelitis (EAE) to explore the underlying immune mechanisms of EAE. Our results showed that the levels of CCL26 and CCR3 in EAE rats were significantly increased compared with those in the control group. 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. We concluded that CCL26, which in turn binds to the receptor CCR3, showed pro-inflammatory effects and aggravated tissue damage involving BBB impairment, especially in the acute stage of EAE. Our study uncovers another possible immunopathological mechanism of MS and provides a possible target for immune therapy.