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dc.contributor.authorDincel, Gungor Cagdas
dc.contributor.authorAtmaca, Hasan Tarik
dc.date.accessioned2021-11-09T19:42:34Z
dc.date.available2021-11-09T19:42:34Z
dc.date.issued2015
dc.identifier.issn0014-4894
dc.identifier.issn1090-2449
dc.identifier.urihttps://doi.org/10.1016/j.exppara.2015.06.009
dc.identifier.urihttps://hdl.handle.net/20.500.12440/3417
dc.description.abstractToxoplasma 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 to identify any correlation between toxoplasmosis neuropathology and investigate the consequences of the cellular responses protect against T. gondii. Mice were infected with ME49 strain T. 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 30 and 60 days post infection. Results of the study revealed that the levels of eNOS (p < 0.05), nNOS (p < 0.05), iNOS (p < 0.005), GFAP (p < 0.005) and NF (p < 0.005) were remarkably higher in T. gondii-infected mice than in uninfected control. The most prominent finding from our study was 10 and 30 days after inoculation data indicating that increased levels of 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 high expressed NO origin was not only inducible nitric oxide synthase but also endothelial and neuronal. We demonstrated that activation of astrocytes and microglia/macrophages is a significant event in toxoplasma encephalitis (TE). The results also clearly indicated that increased levels of NO might contribute to neuropathology related with TE. Furthermore, expression of NF might gives an idea of the progress and critical for diagnostic significance of this disease. (C) 2015 Elsevier Inc. All rights reserved.en_US
dc.description.sponsorshipGumushane Univesity, Scientific Research CouncilGumushane University [13.B0421.02.1]en_US
dc.description.sponsorshipThis work was supported by grants from Gumushane Univesity, Scientific Research Council (Project no: 13.B0421.02.1). This study was presented as an oral presentation in 3rd International Conference & Exhibition on Pathology Congress 2014, San Antonio, USA.en_US
dc.language.isoengen_US
dc.publisherAcademic Press Inc Elsevier Scienceen_US
dc.relation.ispartofExperimental Parasitologyen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectToxoplasma gondiien_US
dc.subjectNitric oxideen_US
dc.subjectNeuropathologyen_US
dc.subjectNeurofilamenten_US
dc.subjectGlial fibrillary acidic proteinen_US
dc.titleNitric oxide production increases during Toxoplasma gondii encephalitis in miceen_US
dc.typearticleen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.description.wospublicationidWOS:000360323400014en_US
dc.description.scopuspublicationid2-s2.0-84934277166en_US
dc.departmentGümüşhane Üniversitesien_US
dc.authoridDINCEL, Gungor Cagdas / 0000-0002-6985-3197
dc.authoridDINCEL, Gungor Cagdas / 0000-0002-6985-3197
dc.authoridATMACA, HASAN TARIK / 0000-0001-8379-4114
dc.identifier.volume156en_US
dc.identifier.startpage104en_US
dc.identifier.doi10.1016/j.exppara.2015.06.009
dc.identifier.endpage112en_US
dc.authorwosidDINCEL, Gungor Cagdas / AAF-3830-2020
dc.authorwosidDINCEL, Gungor Cagdas / H-7026-2018
dc.authorscopusid54784389100
dc.authorscopusid36778766400
dc.description.pubmedpublicationidPubMed: 26115941en_US


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