{"title":"Toxoplasma gondii modulates immune responses and mitigates type 1 diabetes progression in a streptozotocin-induced rat model.","authors":"Kimia Moradi, Reyhaneh Moghaddami, Arshad Ghaffari-Nasab, Monir Khordadmehr, Abdol Sattar Pagheh, Hossein Mosajakhah, Sahar Rezaei, Esmaeil Gharepapagh, Mahdi Ahmadi, Mahbobeh Montazeri, Hossein Pazoki, Ehsan Ahmadpour","doi":"10.1186/s12964-025-02168-1","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"172"},"PeriodicalIF":8.2000,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Communication and Signaling","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s12964-025-02168-1","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
期刊介绍:
Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior.
Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.