Kronik Toksoplazmoz Modelinde Erken Dönem Bağışıklık Yanıtının Değerlendirilmesi

Ensefalitik toksoplazmoz, Toxoplasma gondii tarafından oluşturulan, ölümcül sonuçları olabilen ve özellikle de immun-baskılanmış bireylerin etkilendiği bir hastalıktır. Ancak insan çalışmalarının sınırlı olmasından dolayı konak- patojen ilişki mekanizmasının aydınlatılması için en iyi alternatif, deneysel fare çalışmaları olmaktadır. C57BL/6 fareler toksoplazmoza duyarlıdır ve T. gondii ile oluşan enfeksiyonlarında herhangi bir immun baskılayıcı etkiye maruz kalmadan da ensefalitik toksoplazmoz geliştirebilirler. Bu nedenle de özellikle T. gondii’ nin ME49 gibi tip II suşlarıyla oluşturulan immunopatogenez ve mekanizma çalışmalarında tercih edilmektedirler. Sunulan bu çalışmada; proinflamatuar sitokinler; İnterleukin- 12 IL-12 , İnterferon-γ IFN-γ ve Tümör Nekrozis Faktör-α TNF-α ’ nın, ME49 suşuyla enfekte edilmiş C57BL/ 6 farelerde görülen ensefalitik toksoplazmozdaki rolü araştırılmıştır. Bunun için, enfekte fareler enfeksiyonun 30. gününde sakrifiye edilmiş, hem histopatolojik hem de immunoperoksidaz testler uygulanmıştır. Sonuç olarak, yapılan ayrı ayrı boyamalarda; beyin korteks, amigdala, striatum ve substantia nigradaki T. gondii immunopozitiflikleriyle, IL-12, IFN-γ ve TNF-α sitokin ekspresyonlarının birbirleriyle korelasyon içinde olduğu gösterilmiştir. Sonuç olarak, bu çalışmada elde edilen bulgular, beyinde tip I proinflamatuar sitokinlerin T.gondii enfeksiyonunun erken aşamasında artış gösterdiklerini ortaya koymaktadır. Dipnot: Bu çalışma, çalışmayla Kırıkkale Üniversitesi Sağlık Bilimleri Enstitüsü “FARELERDE KRONİK ENSEFALİTİK Toxoplasma gondii Enfeksiyonunda, Konak-Parazit İlişkisi Ve Konak İmmun Yanıtının Fonksiyonel Nöropatoloji İle Araştırılması” adlı doktora tez çalışmasının ön bulgularını kapsamaktadır ve Kırıkkale Üniversitesi Bilimsel Araştırma Projeleri Birimi, Proje No:2016/ 040 ile desteklenmiştir.

Evaluation of Early Stage Immun Response in Experimental Chronic Toxoplasmosis Model

Encephalitic toxoplasmosis caused by Toxoplasma gondii is a disease that can cause death in immunocomprimised patient. Since experimental human studies are limited, experimental murine models are the most functional way for enlightening the mechanism of the host- pathogen interactions. C57BL/ 6 mice are susceptible for the toxoplasmosis compared the other mouse species. They may develop encephalitic toxoplasmosis without any immunocomprimised disease. Therefore, they generally infected with T. gondii for the host- pathogen interaction and immunopathogenesis studies. In present study, we investigate the role of the pro-inflammatory cytokines such as Interleukin- 12 IL-12 , Interferon-γ IFN-γ and Tumor Necrosis Factor-α TNF-α in ME49 infected C57BL/6 mice. ME49 infected mice sacrified at post-infection 30 days, then histopathological and immunoperoxidase tests applied for the cytokines and T. gondii antigen. Thus, there were T. gondii immunopositivity detected in cortex, amygdala, hippocampus, striatum and substantia nigra. IL-12, IFN-γ and TNF-α expressions showed correlation in those examined areas. In this context, it is thought that Type I proinflammatory cytokin levels are prominently increased during the early stage of encephalitic toxoplasmosis.

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