Parasite and host defense mechanisms: whenToxoplasma subjugates the brain

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Abstract Brain is an immune-privileged organ for infection with the neurotropic protozoan parasite, Toxoplasma gondii. T. gondii escapes the immune system by establishing a dormant and lifelong bradyzoite cyst during chronic and latent phases within the brain and musculature of immunocompetent individuals. During acute stage T. gondii stimulates the host defense to display depressive behaviors over a background of sickness. Infection with T. gondii is initiated with its proliferative tachyzoite that acts on peripheral immune cells to produce the pro-inflammatory cytokines, most of them induce the behavioral signs of sickness. For instance, interleukin-(IL) 1β, tumor necrosis factor-α and IL-6 are triggering most of sickness symptoms. Whereas, the cardinal inflammatory cytokine interferon-γ activates, indoleamine 2,3 dioxygenase (IDO), an enzyme mainly synthesized by phagocytic cells like macrophages and microglia. IDO activation causes tryptophan depletion and precipitates the depressive symptoms. On other hand, brain encysting with the bradyzoite is characterized by immunosuppression in form of reduced pro-inflammatory and heightened anti-inflammatory responses as evidenced by increased phagocytic activity and release of IL-10 and TGF-β. To conclude, T. gondii has multiple strategies to harness the host’s immune mechanisms and behavior by the virtue of dual effects of tachyzoite-induced immune invasion intertwined with bradyzoite-induced immune evasion.

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