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Nitric Oxide Expression Increase During in Chronic Toxoplasma gondii Encephalitis in Mice

Gungor Cagdas Dincel

Nitric Oxide Expression Increase During in Chronic Toxoplasma gondii Encephalitis in Mice

Gungor Cagdas Dincel Gumushane University Laboratory and Veterinary Health Program, Turkiye


Gungor Cagdas Dincel has completed Doctor of Science in Veterinary Medicine, Doctoral Thesis: \'Apoptosis of Central Nervous System in Border Disease Infected Small Ruminanats\'. His main research area has been so far Experimental Toxoplasmosis in laboratory animals. He mastered the techniques such as immunohistochemistry, cell culture and molecular pathology. He is the Head of Veterinary department and College Vice Director as a Asistant Professor of Siran Mustafa Beyaz Vocational High School since 2012. He is responsible for the Immunopathology Laboratory of the Gumushane University. His fields of research - pathologies of the central nervous system. He had published five papers in reputed journals.


Toxoplasma gondii is an intracellular parasite with the potential of causing severe encephalitis among immunocompromised human and animals. The aim of this experimental study was to investigate the immunomodulatory and immunopathological role of Nitric oxide (NO) in central nervous systems and the consequences of the cellular responses protect against Toxoplasma gondii. Mice were infected with ME49 Strain Toxoplasma gondii and levels of endothelial, neuronal and inducible nitric oxide synthase (eNOS, nNOS, iNOS), Glial Fibrillary Acidic Protein (GFAP) and Neurofilament (NF) were examined in brain tissues by immunohistochemistry, during the development and establishment of a chronic infection at 10 days, 1 and 2 months post infection. Results revealed that the levels of eNOS (p<0,05), nNOS (p<0.05), iNOS (p<0.05), GFAP (p<0.01) and NF (p<0.05) were remarkably higher in Toxoplasma gondii-infected mice than in uninfected controls mice. In this study 10 and 30 days after inoculation data indicating that NO not only a potential neuroprotective role for immunoregulatory and immunopathological but also might be a molecular trigger of bradyzoite development. Furthermore, this findings were shown that expressed of NO origin is not only inducible nitric oxide synthase but also endothelial and neuronal. We demonstrated that cerebellar cells especially astrocyte and microglia activation is a significant of Toxoplasma encephalitis. In addition to these comments, expression of NF might give an idea of the progress of the disease.

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