Pathogenetic mechanism and construct of neuromyelitis optica model by immunization activation

Objective: To obtain a mouse model that is clinically similar to neuromyelitis optica (NMO) via immunization.Methods: In this study, C57BL/6 mice were co-immunized by injecting human complement and aquaporin 4 (AQP4) antibody against NMO in the lateral ventricle, and the animals’ immune response was strengthened by injection of myelin glial cell glycoprotein and interleukin (IL)-17A and Bacilus Calmete-Guerin vaccine. To obtain a mouse model of autoimmune encephalomyelitis, after obtaining a model mouse with stable symptoms, we identified its behavioral performance, pathology, immunohistochemistry, molecular biology, and electrophysiology.Results: The behavioral observation showed that the model mice were similar to NMO patients in terms of limb symptoms and optic nerve performance. Regarding the pathology and immunohistochemistry, the spinal cords of model mice had obvious demyelination and AQP4 and glial fibrillary acid protein expression changes. Moreover, it was found that the inflammatory factors of the model mice, i.e., IL-1 and IL-17, were significantly expressed. In the detection of visual evoked potentials, we used the flash evoked potential detection method to demonstrate that the model and control groups had significantly longer S1 and T wave incubation periods, with significant differences.Conclusion: This research revealed that the mouse model of autoimmune encephalomyelitis prepared by this method is similar to the characteristics of NMO.