Background/Objectives: The coccidian protozoan Toxoplasma gondii (T. gondii) is among the most prevalent zoonotic parasites worldwide. Nitric oxide (NO) production by macrophages is considered a critical microbicidal mechanism against various intracellular pathogens, including T. gondii. While the role of the inducible nitric oxide synthase isoenzyme (iNOS) has been widely investigated in both acute and chronic T. gondii infections, the specific functions of the neuronal (nNOS) isotype in the antiparasitic immune response, particularly during chronic toxoplasmosis, remain largely uncovered. Hence, this report seeks to bridge the gap regarding the potential participation of nNOS in experimental chronic T. gondii infection. Methods: The study included 56 Swiss albino mice, equally allocated into four experimental groups: (G1) negative control, (G2) infected control, (G3) infected-L-arginine-treated, and (G4) infected-7-Nitroindazole-treated. All groups except (G1) were orally infected with the avirulent (ME49) T. gondii strain. Nine weeks post-infection, all mice were euthanized for parasitological, histopathological, immunohistochemical, and biochemical analyses. Results: The NO donor, L-arginine, induced a significant reduction in the number of T. gondii cysts, together with strong nNOS immunoreactivity in the brain sections of the treated mice. Conversely, the highest parasitic burden was observed following selective nNOS inhibition with 7-Nitroindazole, exacerbating parasite-induced pathology. Conclusions: The neuronal isotype serves as a critical source of NO production during the chronic stage of T. gondii infection, thereby enhancing parasite elimination and contributing to host tissue protection.
Marwa Omar (Fri,) studied this question.
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