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NADPH phagocyte oxidase knockout mice control trypanosoma cruzi proliferation,but develop circulatory collapse and succumb to infection
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نویسنده
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santiago h.c. ,lombana c.z.g. ,macedo j.p. ,utsch l. ,tafuri w.l. ,campagnole-santos m.j. ,alves r.o. ,alves-filho j.c.f. ,romanha a.j. ,cunha f.q. ,teixeira m.m. ,radi r. ,vieira l.q.
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منبع
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plos neglected tropical diseases - 2012 - دوره : 6 - شماره : 2
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چکیده
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•no is considered to be a key macrophage-derived cytotoxic effector during trypanosoma cruzi infection. on the other hand,the microbicidal properties of reactive oxygen species (ros) are well recognized,but little importance has been attributed to them during in vivo infection with t. cruzi. in order to investigate the role of ros in t. cruzi infection,mice deficient in nadph phagocyte oxidase (gp91 phox-/- or phox ko) were infected with y strain of t. cruzi and the course of infection was followed. phox ko mice had similar parasitemia,similar tissue parasitism and similar levels of ifn-γ and tnf in serum and spleen cell culture supernatants,when compared to wild-type controls. however,all phox ko mice succumbed to infection between day 15 and 21 after inoculation with the parasite,while 60% of wild-type mice were alive 50 days after infection. further investigation demonstrated increased serum levels of nitrite and nitrate (nox) at day 15 of infection in phox ko animals,associated with a drop in blood pressure. treatment with a nos2 inhibitor corrected the blood pressure,implicating nos2 in this phenomenon. we postulate that superoxide reacts with •no in vivo,preventing blood pressure drops in wild type mice. hence,whilst superoxide from phagocytes did not play a critical role in parasite control in the phox ko animals,its production would have an important protective effect against blood pressure decline during infection with t. cruzi. © 2012 santiago et al.
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آدرس
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departamento de bioquímica e imunologia,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais,brazil,laboratory of parasitic diseases,national institutes of health,bethesda,md, United States, departamento de bioquímica e imunologia,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais,brazil,department of pathobiology,school of veterinary medicine,university of pennsylvania,philadelphia,pa, United States, departamento de bioquímica e imunologia,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais, Brazil, departamento de bioquímica e imunologia,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais, Brazil, departamento de patologia geral,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais, Brazil, departamento de fisiologia e biofísica,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais, Brazil, centro de pesquisas rené rachou,fiocruz,belo horizonte,minas gerais, Brazil, departmento de bioquímica e imunologia,faculdade de medicina de ribeirão preto,universidade de são paulo,ribeirão preto, Brazil, centro de pesquisas rené rachou,fiocruz,belo horizonte,minas gerais, Brazil, departmento de bioquímica e imunologia,faculdade de medicina de ribeirão preto,universidade de são paulo,ribeirão preto, Brazil, departamento de bioquímica e imunologia,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais, Brazil, departamento de bioquímica,universidad de la república,montevideo,uruguay,center for free radical and biomedical research,universidad de la república,montevideo, Uruguay, departamento de bioquímica e imunologia,instituto de ciências biológicas,universidade federal de minas gerais,belo horizonte,minas gerais,brazil,núcleo de pesquisas em ciências biológicas,universidade federal de ouro preto,ouro preto,minas gerais, Brazil
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Authors
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