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

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

PMC · DOI: 10.1007/s11686-025-01035-w · Acta Parasitologica · 2025-04-29

## TL;DR

This study shows that Schistosoma mansoni egg antigens may help treat type 1 diabetes by reducing inflammation and improving blood sugar control in mice.

## Contribution

The novel finding is that SEA treatment modulates immune responses and improves metabolic outcomes in a T1D mouse model.

## Key findings

- SEA treatment increased regulatory T cells and immunosuppressive markers like TGF-β and FOXp3.
- SEA reduced inflammation and improved glycemic control in diabetic mice.
- Immune modulation by SEA shifted responses toward anti-inflammatory Th2 profiles.

## Abstract

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.

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.

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.

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.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), TGFB1 (transforming growth factor beta 1), FOXP3 (forkhead box P3), IL4 (interleukin 4), IL10 (interleukin 10)
- **Chemicals:** streptozotocin (PubChem CID 29327), phosphate-buffered saline (PubChem CID 24978514)
- **Diseases:** type 1 diabetes (MONDO:0005147), T1D (MONDO:0005147)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Il4 (interleukin 4) [NCBI Gene 16189] {aka BSF-1, Il-4}, Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Foxp3 (forkhead box P3) [NCBI Gene 20371] {aka JM2, scurfin, sf}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}
- **Diseases:** inflammation (MESH:D007249), T1D (MESH:D003922), Diabetic (MESH:D003920)
- **Chemicals:** STZ (MESH:D013311), blood glucose (MESH:D001786), PBS (-)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12041111/full.md

## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC12041111/full.md

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Source: https://tomesphere.com/paper/PMC12041111