Correlation analysis of pathogenesis of optic neuritis with helper T cell subsets in a mouse experimental autoimmune encephalomyelitis model / 中国组织工程研究

ABSTRACT

BACKGROUND:More and more evidence have shown that autoimmune-induced inflammatory demyelinating mostly leads to optic neuritis that is quite an early manifestation of multiple sclerosis, but whether the pathogenesis of optic neuritis in experimental autoimmune encephalomyelitis (EAE) mice is correlated with helper T cellsubsets has rarely been reported. OBJECTIVE:To analyze the correlation between pathogenesis of optic neuritis of mouse EAE model with helper T cellsubsets. METHODS:The mice were injected intraperitoneal y Bordetel a pertussis to establish EAE models. Then, the animal models were subjected to immunization for 11, 15, 19 days, respectively. Mice undergoing intraperitoneal injection of normal saline served as controls (adjuvant group). RESULTS AND CONCLUSION:Compared with the adjuvant group, the protein expression of interleukin 4 in the optic nerve decreased in the 19-day immunization group (P<0.05);the protein expression of interleukin 17 in the optic nerve increased in the 11-and 15-day immunization groups (P<0.05);the protein expression of interferonγin the optic nerve increased in the 15-and 19-day immunization groups (P<0.05);the protein expression of Foxp3 in the optic nerve decreased in the 11-, 15-and 19-day immunization groups (P<0.05). Real-time PCR results showed that compared with the adjuvant group, the mRNA expression of interferonγand Foxp3 in the optic nerve decreased (P<0.05), while mRNA expression of RORt increased in the 11-, 15-and 19-day immunization groups;the mRNA expression of interleukin 4, interleukin 17, T-beat increased in the 15-and 19-day immunization groups (P<0.05);the mRNA expression of GATA3 reduced in the 19-day immunization group (P<0.05). These results reveal that Foxp3 expression and helper T cellreduction have important influences on the development of optic neuritis in EAE mouse models, interleukin 17 may mediates inflammatory injury in the early stage, while interferon-γmakes inflammatory injury worse in the peak incidence of the disease.