Temporal Neuroimmune Changes During Primary and Persistent Experimental Toxoplasmic Encephalitis

Toxoplasma gondii persists in the central nervous system and may cause severe toxoplasmic encephalitis, particularly in immunocompromised hosts. Our previous studies demonstrated that T. gondii-induced neuropathology involves oxidative and nitrosative stress, apoptosis, glial activation, blood–brain barrier injury, and GMF-β- and SAP/NF-κB-associated responses. This study investigated the temporal immunoreactivity of CD68, S100B, Foxp3, and IL-5 during early and chronic experimental infection. Twenty-four female Swiss albino mice were assigned to one uninfected control group and three ME49-infected groups examined at 10, 30, and 60 days post-infection (n = 6/group). Marker immunoreactivity was evaluated by immunohistochemistry and quantitative image analysis. CD68 immunoreactivity was markedly increased at day 10, rose further by day 30, and remained high at day 60. In contrast, immunoreactivity for S100B, Foxp3, and IL-5 was limited at day 10 but increased markedly at days 30 and 60. Most notably, IL-5 continued to increase significantly from day 30 to day 60, whereas CD68, S100B, and Foxp3 remained at similarly high levels during this interval. These temporally divergent patterns demonstrate an early myeloid/phagolysosomal response followed by established astroglial, Foxp3-associated regulatory, and cytokine-associated tissue responses. The continued increase in IL-5, together with persistent neuropathological changes, supports the interpretation that late chronic toxoplasmic encephalitis is an active rather than quiescent neuroimmunopathological phase.