Impact of Toxoplasma gondii infection on adipokine secretion and the regulation of inflammatory cytokines in the host
Abstract
Toxoplasma gondii infection disrupts host metabolic and immune homeostasis by altering adipokine secretion and modulating the balance between pro- and anti-inflammatory cytokines, potentially contributing to systemic inflammation and metabolic dysfunction. This study aimed to investigate the effects of T. gondii infection on host adipokine secretion and inflammatory cytokine regulation. A six-month case-control study (January–June 2025) was conducted at Al-Habbobi Teaching Hospital, involving 100 T. gondii seropositive patients and 50 matched healthy controls aged 18–60. Exclusion criteria included pregnancy, immunosuppressive or lipid-lowering therapy, and chronic inflammatory or autoimmune diseases. Following overnight fasting, 5 mL venous blood samples were collected, serum separated, and stored at –20 °C. Levels of adipokines (leptin, adiponectin, resistin) and cytokines (TNF-α, IL-6, CRP, IL-10, TGF-β) were measured using ELISA kits (Bio-Techne, USA). No significant differences in age, sex, residence, or smoking status were observed b e tween groups ( P > 0.05), but BMI was significantly higher in patients ( P = 0.003). Patients exhibited significantly i n creased leptin and resistin ( P < 0.001) and decreased adiponectin ( P < 0.001). Pro-inflammatory cytokines TNF-α, IL-6, and CRP were elevated ( P < 0.001), whereas anti-inflammatory IL-10 and TGF-β were reduced ( P < 0.001). There were strong positive relationships between leptin- TNF- 2, adiponectin- IL-10, and resistin-CRP ( P < 0.001). The infection of T. gondii greatly changes the secretion of adipokines and cytokine balance, which favors systemic inflammation and the inability to regulate the immune system, presumably through the effect of parasite-induced immune and metabolic alter a tions.References
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