Purpose <p>This study aimed to investigate the effects of <i>Schistosoma mansoni</i> soluble egg antigen (SEA) on type 1 diabetes (T1D) in a streptozotocin (STZ)-induced diabetic mouse model.</p> Methods <p>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.</p> Results <p>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.</p> Conclusion <p>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.</p>

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Impact of Soluble Schistosomal Egg Antigens on Type 1 Diabetes Mellitus in an Induced Diabetic Mouse Model

  • Mohammed Y. Shakra,
  • Morsy R. M. Geneedy,
  • Haitham Kh. Ahmad,
  • Moamen A.I. Mazen,
  • Mostafa E. Mostafa

摘要

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.