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Updated: Sep 27, 2026

Using Eggs from Schistosoma mansoni as an In vivo Model of Helminth-induced Lung Inflammation
Published on: June 5, 2012
Effect of schistosoma mansoni egg deposition on multiple low doses streptozotocin induced insulin dependent diabetes
Hala S El-Wakil1, Tarek S E Aboushousha, Omkolsoum El Haddad
1Department of Parasitology, Faculty of Medicine, Ain Shams University, Cairo 11566, Egypt.
Abstract:
To explore the role of Schistosoma mansoni infection in the prevention of autoimmune mediated insulin dependant diabetes mellitus, we examined the effects of multiple low doses of the pancreatic islets beta cell toxin, streptozotocin (STZ) 40mg/kg body weight i.p., given 8 weeks post infection, period of S. mansoni egg deposition, on S. mansoni infected C57BL/6J mice, in comparison to non-infected STZ given group. Mice treated with STZ (G III) became gradually hyperglycemic reaching highest level on days 17 post STZ with mean blood glucose level of 334.9 +/- 14.9 vs 130.3 +/- 9.2 mg/dl in control group (G IV). S. mansoni infection (G II) significantly reduced the elevation in blood glucose levels from days 7 post STZ onwards reaching 224mg/dl +/- 12.7 on days 17 (P < .0.001). Morphologic examination of pancreas on day 21 post STZ, revealed that the non-infected STZ (G III) given mice had significantly smaller mean islets area (5,060.51 mu2 +/- 1,567.28) and significantly fewer mean number of beta cells/islets (76.23 +/- 19.18) than the infected STZ given group (G II) which had mean islets area (9,305. 3l mu2 +/- 3,277.59) and 116.75 +/- 27.27 beta-cells/islets. Pancreatic tissue revealed also focal degeneration in the cells of islets of Langrhans in the non-infected STZ given mice (G III), in comparison, to the infected STZ given group (G II). which had much less evident cells degeneration. These findings revealed that S. mansoni egg deposition which leads to a shift from Th1 (IFN-gamma mainly) to Th2 (IL4, IL5, IL10 and TGF-beta cytokine profiles causes down-regulation of the Th1 cell mediated autoimmune insulin dependant diabetes mellitus (IDDM). On the other hand, S. mansoni eggs excretions were significantly lower in the infected STZ given group (G II) than the infected group (G I). This finding may be the result of impaired maturation of egg in diabetic mice. It is concluded that the modulation of immune response in S. mansoni infected mice with S. mansoni egg deposition, can suppress the autoimmune type 1 insulin dependant diabetes mellitus induced by multiple low doses streptozotocin.
Insights
Schistosoma mansoni infection protects against autoimmune diabetes by modulating the immune response. This parasitic infection, specifically S. mansoni egg deposition, down-regulates Th1-mediated autoimmune diabetes and preserves pancreatic beta cells.
Area of Science:
- Immunology
- Parasitology
- Endocrinology
Background:
- Autoimmune diabetes, or type 1 diabetes, is an immune-mediated disease.
- Schistosoma mansoni infection is known to modulate host immune responses.
Purpose of the Study:
- To investigate the protective role of Schistosoma mansoni infection against streptozotocin-induced autoimmune diabetes in mice.
Main Methods:
- Mice were infected with Schistosoma mansoni and later treated with multiple low doses of streptozotocin (STZ).
- Blood glucose levels and pancreatic islet morphology were assessed and compared between infected and non-infected groups.
Main Results:
- Schistosoma mansoni infection significantly reduced hyperglycemia and preserved pancreatic beta cells in STZ-treated mice.
- Infection led to a shift in immune response from Th1 to Th2, down-regulating autoimmune diabetes.
- Egg excretion was lower in diabetic mice, possibly due to impaired egg maturation.
Conclusions:
- Schistosoma mansoni infection, particularly egg deposition, can suppress autoimmune type 1 diabetes.
- Immune modulation by S. mansoni offers a potential strategy for managing autoimmune diabetes.
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