Acta parasitologica · 2025
Impact of Soluble Schistosomal Egg Antigens on Type 1 Diabetes Mellitus in an Induced Diabetic Mouse Model.
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Shakra Mohammed Y, Geneedy Morsy R M, Ahmad Haitham Kh, Mazen Moamen A I, Mostafa Mostafa E
Аннотация
PURPOSE: This study aimed to investigate the effects of Schistosoma mansoni soluble egg antigen (SEA) on type 1 diabetes (T1D) in a streptozotocin (STZ)-induced diabetic mouse model.
METHODS: The study examined the effects of Schistosoma mansoni soluble egg antigen (SEA) on type 1 diabetes (T1D) using a mouse model, involving 50 mice divided into three groups: a healthy control group receiving phosphate-buffered saline (PBS), a diabetic control group with STZ-induced T1D also receiving PBS, and a diabetic treated group receiving SEA. Biochemical and immunological analyses were conducted on blood samples collected at four and eight weeks post-treatment to assess metabolic markers like blood glucose and insulin levels, as well as immune markers including TNF-α, TGF-β, FOXp3, IL-4, and IL-10.
RESULTS: SEA treatment induced early immune modulation at four weeks and sustained metabolic and immunological improvements at eight weeks, marked by increased regulatory T cells (elevated FOXp3), activation of immunosuppressive pathways (increased TGF-β), reduced inflammation (decreased TNF-α), a shift to an anti-inflammatory Th2 response (elevated IL-4 and IL-10), improved glycemic control, lower blood glucose levels, and higher insulin levels.
CONCLUSION: SEA exhibits potential therapeutic effects against T1D by modulating immune responses, promoting Th2 polarization, and increasing regulatory T cell activity. This immunological shift reduces systemic inflammation and enhances glycemic control.
METHODS: The study examined the effects of Schistosoma mansoni soluble egg antigen (SEA) on type 1 diabetes (T1D) using a mouse model, involving 50 mice divided into three groups: a healthy control group receiving phosphate-buffered saline (PBS), a diabetic control group with STZ-induced T1D also receiving PBS, and a diabetic treated group receiving SEA. Biochemical and immunological analyses were conducted on blood samples collected at four and eight weeks post-treatment to assess metabolic markers like blood glucose and insulin levels, as well as immune markers including TNF-α, TGF-β, FOXp3, IL-4, and IL-10.
RESULTS: SEA treatment induced early immune modulation at four weeks and sustained metabolic and immunological improvements at eight weeks, marked by increased regulatory T cells (elevated FOXp3), activation of immunosuppressive pathways (increased TGF-β), reduced inflammation (decreased TNF-α), a shift to an anti-inflammatory Th2 response (elevated IL-4 and IL-10), improved glycemic control, lower blood glucose levels, and higher insulin levels.
CONCLUSION: SEA exhibits potential therapeutic effects against T1D by modulating immune responses, promoting Th2 polarization, and increasing regulatory T cell activity. This immunological shift reduces systemic inflammation and enhances glycemic control.