Relação entre imunomarcação para iNOS, carga parasitária, parasitemia e lesões em diferentes órgãos de ratos wistar experimentalmente infectados com Trypanosoma evansi
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Data
2017-11-20
Autores
Pereira, Priscila Préve
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Universidade Estadual Paulista (Unesp)
Resumo
Trypanosoma evansi acomete diversas espécies de animais em todo o mundo. A infecção se caracteriza por intensa parasitemia associada a anemia, que evolui para lesões teciduais atribuídas à resposta autoimune do hospedeiro. O objetivo desse estudo foi avaliar a evolução da infecção experimental pelo Trypanosoma evansi até as fases mais tardias da infecção, a partir das lesões patológicas, estresse oxidativo tecidual, parasitemia e parâmetros hematológicos. Para tal, os ratos infectados com T. evansi foram eutanasiados aos 7, 14, 21, 28 e 35 dias após a inoculação (DAI), os animais foram anestesiados, e posteriormente colhidos 5 ml de sangue intracardíaco com anticoagulante etileno diamino tetra acetato de sódio (EDTA). Os achados histopatológicos foram avaliados de acordo com o tipo de lesão e a incidência de T. evansi, sendo descrita a localização da lesão e determinada a intensidade por escores. O estresse oxidativo foi avaliado a partir da resposta imune celular por imunomarcações da enzima óxido nítrico sintase induzível (iNOS) de imunohistoquímica. A carga parasitária foi detectada pela imunomarcação do parasita pela mesma técnica. Foi notada uma acentuada anemia no DAI 21. No baço, a hiperplasia linfoide em todos os momentos, evidenciando-se no DAI 35. No coração, presença de parasitas no interior de vasos e câmaras ventriculares, no DAI 21 e infiltrado inflamatório polimorfonuclear em todos os momentos, porém, extremamente acentuado no DAI 28. Nos rins notou-se a presença do parasita a partir do DAI 14 associado a uma nefrose tóxica. Nos pulmões poucos parasitas, espessamento de septos alveolares, hemorragia em todo período da infecção e infiltrado inflamatório polimorfonuclear. Nos linfonodos poplíteos com parasitas a partir do DAI 28 e intensa presença de mastócitos (MCs) em DAI 21. No encéfalo, foi observado a descontinuidade da barreira hematoencefálica, em DAI 21. Os resultados foram importantes para elucidar a infeção por tripanossomíases, e o hospedeiro nos diferentes momentos diante desse cenário. Em todos os órgãos foram detectados a presença de parasita por imuno-histoquimica, apresentando maior intensidade em DAI21, e nos próximos momentos reduzindo significamente. Assim como a intensidade de células imunomarcadas para o óxido nítrico foi alta entre DAI14 e DAI 21 e após esse momento reduziram. Os dados mostram que o óxido nítrico pode lesionar os tecidos do hospedeiro como o parasita, e assim reduzindo a carga parasitária.
Trypanosoma evansi affects several species of animals worldwide. The infection is characterized by intense parasitemia associated with anemia, which evolves to tissue lesions attributed to the host's autoimmune response. The objective of this study was to evaluate the evolution of the experimental infection by Trypanosoma evansi until the later stages of the infection, from the pathological lesions, tissue oxidative stress, parasitemia and hematological parameters. To that end, mice infected with T. evansi were euthanized at 7, 14, 21, 28 and 35 days after inoculation (DAI), animals were anesthetized, and 5 ml of intracardiac blood was then collected with anticoagulant ethylene diamine tetraacetate sodium (EDTA). The histopathological findings were evaluated according to the type of lesion and the incidence of T. evansi. The location of the lesion was described and the intensity determined by scores. Oxidative stress was evaluated from the cellular immune response by immunostaining of the enzyme inducible nitric oxide synthase (iNOS) immunohistochemistry. The parasite load was detected by immunolabeling the parasite by the same technique. It was noted a marked anemia in DAI 21. In the spleen, lymphoid hyperplasia at all times, evidenced in DAI 35. In the heart, presence of parasites inside vessels and ventricular chambers, in DAI 21 and polymorphonuclear inflammatory infiltrate in all However, the presence of the parasite from the DAI 14 associated with a toxic nephrosis was observed in the kidneys. In the lungs few parasites, thickening of alveolar septa, hemorrhage throughout the infection period and polymorphonuclear inflammatory infiltrate. In popliteal lymph nodes with parasites from DAI 28 and intense presence of mast cells (MCs) in DAI 21. In the brain, the discontinuity of the blood-brain barrier was observed in DAI 21. The results were important to elucidate the infection by trypanosomiasis, and the different moments in front of this scenario. In all organs the presence of parasite was detected by immunohistochemistry, showing a greater intensity in DAI21, and in the next moments reducing significantly. As well as the intensity of cells immunolabelled for nitric oxide was high between DAI14 and DAI 21 and after that time reduced. The data show that nitric oxide can injure host tissues like the parasite, and thus reduce parasitic burden.
Trypanosoma evansi affects several species of animals worldwide. The infection is characterized by intense parasitemia associated with anemia, which evolves to tissue lesions attributed to the host's autoimmune response. The objective of this study was to evaluate the evolution of the experimental infection by Trypanosoma evansi until the later stages of the infection, from the pathological lesions, tissue oxidative stress, parasitemia and hematological parameters. To that end, mice infected with T. evansi were euthanized at 7, 14, 21, 28 and 35 days after inoculation (DAI), animals were anesthetized, and 5 ml of intracardiac blood was then collected with anticoagulant ethylene diamine tetraacetate sodium (EDTA). The histopathological findings were evaluated according to the type of lesion and the incidence of T. evansi. The location of the lesion was described and the intensity determined by scores. Oxidative stress was evaluated from the cellular immune response by immunostaining of the enzyme inducible nitric oxide synthase (iNOS) immunohistochemistry. The parasite load was detected by immunolabeling the parasite by the same technique. It was noted a marked anemia in DAI 21. In the spleen, lymphoid hyperplasia at all times, evidenced in DAI 35. In the heart, presence of parasites inside vessels and ventricular chambers, in DAI 21 and polymorphonuclear inflammatory infiltrate in all However, the presence of the parasite from the DAI 14 associated with a toxic nephrosis was observed in the kidneys. In the lungs few parasites, thickening of alveolar septa, hemorrhage throughout the infection period and polymorphonuclear inflammatory infiltrate. In popliteal lymph nodes with parasites from DAI 28 and intense presence of mast cells (MCs) in DAI 21. In the brain, the discontinuity of the blood-brain barrier was observed in DAI 21. The results were important to elucidate the infection by trypanosomiasis, and the different moments in front of this scenario. In all organs the presence of parasite was detected by immunohistochemistry, showing a greater intensity in DAI21, and in the next moments reducing significantly. As well as the intensity of cells immunolabelled for nitric oxide was high between DAI14 and DAI 21 and after that time reduced. The data show that nitric oxide can injure host tissues like the parasite, and thus reduce parasitic burden.
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Palavras-chave
Imunohistoquímica, Óxido nítrico, Parasitemia, Radicais livres, Trypanosomíases