Shakra Mohammed Y, Geneedy Morsy R M, Ahmad Haitham Kh, Mazen Moamen A I, Mostafa Mostafa E
Department of Parasitology, Faculty of Medicine, Al-Azhar University, Damietta, Egypt.
Department of Parasitology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
Acta Parasitol. 2025 Apr 29;70(3):98. doi: 10.1007/s11686-025-01035-w.
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.
本研究旨在探讨曼氏血吸虫可溶性虫卵抗原(SEA)对链脲佐菌素(STZ)诱导的糖尿病小鼠模型中1型糖尿病(T1D)的影响。
本研究使用小鼠模型检测曼氏血吸虫可溶性虫卵抗原(SEA)对1型糖尿病(T1D)的影响,将50只小鼠分为三组:接受磷酸盐缓冲盐水(PBS)的健康对照组、患有STZ诱导的T1D且也接受PBS的糖尿病对照组,以及接受SEA的糖尿病治疗组。在治疗后4周和8周采集的血样上进行生化和免疫分析,以评估血糖和胰岛素水平等代谢标志物,以及包括TNF-α、TGF-β、FOXp3、IL-4和IL-10在内的免疫标志物。
SEA治疗在4周时诱导早期免疫调节,并在8周时持续改善代谢和免疫状况,表现为调节性T细胞增加(FOXp3升高)、免疫抑制途径激活(TGF-β增加)、炎症减轻(TNF-α降低)、向抗炎性Th2反应转变(IL-4和IL-10升高)、血糖控制改善、血糖水平降低和胰岛素水平升高。
SEA通过调节免疫反应、促进Th2极化和增加调节性T细胞活性,对T1D具有潜在治疗作用。这种免疫转变可减轻全身炎症并增强血糖控制。