Histopathology of SUMO in TGF-β1 signaling in neural lesions of leprosy reversal reactions

Background Neural lesions are one of the main pathologies occurring in leprosy, which can result in devastating consequences due to disability and deformity. Transforming Growth Factor β (TGF-β) is important in the development of tissue fibrosis. The signaling process for TGF-β starts when it binds to TβRI and TβRII, activating and inducing the phosphorylation of Smad2 and Smad3. SUMOylation is a post-translational modification, mediating the phosphorylation of Smad3 and regulating the TGF-β response. S100b is a marker of nerve damage. Objectives This study evaluates the in-vivo expression levels of SUMO-1 and SUMO-2/3/4, the distribution of Schwann cells and mononuclear cells, and the distribution of S100b and collagen-1 in nerve biopsies of patients with leprosy reversal reactions. Methods Biopsies from twenty-six leprosy patients with reversal reactions (RR) and twenty-four leprosy patients without reversal reactions were stained for SUMO-1, SUMO-2/3/4, S100b, and collagen. We analyzed the cells using a Nikon microscope under 400× magnification. Results We found an increased distribution of SUMO-1, SUMO-2/3/4, macrophages, S100b, and collagen staining in neural lesions of reversal reaction patients, compared to leprosy patients without reversal reactions. Conclusion TGF-β plays an important role in the development of fibrosis in the neural lesions of patients with leprosy. Regulation of the transcription process is mediated by TGF-β1 signaling by SUMO-1 and/or SUMO-2/3/4. The increase in macrophages and collagen, with the decrease in S100b, in patients with neural lesions reflects the damage to nerves in leprosy reversal reactions.