Toxoplasma gondii modulates immune responses and mitigates type 1 diabetes progression in a streptozotocin-induced rat model.

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by the destruction of insulin-producing β-cells in the pancreas. Emerging evidence suggests that infections, including Toxoplasma gondii (T. gondii), may modulate immune responses and influence disease outcomes. This study aimed to investigate the effects of T. gondii infection on the development of T1DM in a Streptozotocin (STZ)-induced rat model, with an emphasis on immune modulation, cytokine profiles, and organ inflammation. In rats experimentally infected with pathogenic and non-pathogenic Toxoplasma strains, diabetes was induced via STZ injection and compared to a control group. Blood glucose levels and the expression of IL-10, IL-1β, and TNF-α at both gene and protein levels were assessed. Histopathological examinations of the pancreas and kidneys were conducted, alongside small-animal PET scans to evaluate metabolic activity in these organs. The T. gondii-infected diabetic groups showed reduced blood glucose levels, increased IL-10, and decreased TNF-α and IL-1β levels compared to the STZ group. Histopathological and PET imaging analyses revealed improved pancreatic and renal tissues and reduced metabolic activity, indicating improvement effects associated with decreased inflammation and immune modulation. T. gondii infection seems to influence immune responses and slow the progression of T1DM in a rat model. These results suggest a potential therapeutic role for parasitic infections in autoimmune diseases, offering valuable insights into the complex relationship between infections, immune regulation, and metabolic health.