Evaluating the potential of Schistosoma mansoni Soluble Egg Antigen (SEA) and Glycoproteins (IPSE and Omega-1) in Inhibiting the Progression of Type 1 Diabetes

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Background Type 1 diabetes (T1D) is characterized by the immune-mediated destruction of pancreatic beta cells, resulting in insulin deficiency and hyperglycemia. Existing insulin therapies manage symptoms but do not fully stabilize blood glucose levels. Schistosoma mansoni infection or its eggs inhibit T1D in rodent models. This study evaluated the antidiabetic effects of Schistosoma mansoni-derived soluble egg antigen (SEA) and glycoproteins (IPSE and Omega-1) in a streptozotocin-induced diabetic rat model. Methods Glycoproteins were designed using in silico methods and synthesized following epitope prediction, antigenicity assessment, and molecular docking analysis. These glycoproteins were administered at doses of 50 μg and 100 μg per rat in a stratified randomized trial comprising eight treatment groups and two control groups, each containing five streptozotocin-induced diabetic rats: SEA (A-B), Omega-13 (C-D), IPSE2-3 (E-H), insulin-only (I), and PBS (J). Blood glucose, weight, IFN-γ, IL-4 levels, and pancreatic histology were assessed. Results In silico analysis of IPSE and Omega-1 showed strong antigenicity (epitopes >0.60), binding energies from -7.9 to -11.9 Kcal/mol, molecular weights of 1261.40–2034.30 Da, and theoretical pI of 8.23–9.70. In vivo, IPSE and Omega-1 significantly reduced glucose (from 5.76–26.16 mmol/L to 3.94–18.92 mmol/L, p < 0.05), promoted weight gain (192.3–235 g to 231.3–250.2 g), and caused mild-moderate pancreatic infiltration. Conclusions These findings suggest that SEA, IPSE, and Omega-1 are promising candidates for novel diabetes therapies, warranting further investigations.

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