The Dynamic Expression Of Canonical Wnt/Beta-Catenin Signalling Pathway In The Pathologic Process Of Experimental Autoimmune Neuritis

Background: Guillain-Barre syndrome (GBS), an autoimmune disease and an acute inflammation disorder, is currently the most frequent cause of acute flaccid paralysis worldwide. EAN, an animal model of GBS, is a CD4+ T cell-mediated autoimmune disease of the PNS. Wnt/beta-catenin signals are critically important to several fundamental aspects of peripheral nerve development and play a crucial role in Schwann cell proliferation. Here, we investigate the role of Wnt/beta-catenin signalling cascades in EAN rats. Methods: 28 male Lewis rats weighing 170 +/- 10 g were randomly divided into control group (n = 7) and EAN groups (Early group; Peak group and Recovery group. n = 7 per group). EAN rats were immunized with P2(57-81) peptide; weighed daily, and the neurologic signs of EAN were evaluated every day. The sciatic nerve was taken on the days 10, 17, and 30 p.i. for H&E staining, transmission electron microscopy and immunohistochemical staining; blood samples were collected weekly from caudal vein to detect IFN-gamma, IL-4, TGF-beta 1; and the sciatic nerve was taken to examinate the dynamics expression of Wnt/beta-catenin pathway molecules. Results: In our study, we chose tail-root injection to better model GBS. Moreover, we observed that IFN-gamma levels paralleled clinical EAN, and the levels of TGF-beta 1 and IL-4 gradually increased and peaked in the recovery phase. In addition, we have shown that canonical Wnt signalling is upregulated and reached a peak in the late recovery phase. Conclusion: Our findings suggest that Wnt/beta-catenin signalling is associated with the promotion of remyelination in EAN rats.