Níveis de TNF-alfa, IL-4 e IL-10 no baço e no fígado de cães naturalmente infectados por Leishmania (Leishmania) chagasi
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Data
2009-10-02
Autores
Michelin, Aparecida de Fátima [UNESP]
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Editor
Universidade Estadual Paulista (Unesp)
Resumo
A leishmaniose visceral canina é causada pela Leishmania (Leishmania) chagasi que é transmitida por flebotomíneos. A evolução clínica desta parasitose depende de uma complexa interação entre o parasita e a resposta imune do hospedeiro. Os cães infectados, que constituem o principal reservatório doméstico desse parasita, podem permanecer assintomáticos ou tornarem-se sintomáticos. O objetivo deste estudo foi quantificar as citocinas TNF- IL-4 e IL-10, em extratos de baço e fígado, de cães naturalmente infectados por L. (L.) chagasi e investigar a ocorrência de associação com a densidade parasitária nestes órgãos. Quarenta cães provenientes da cidade de Araçatuba, estado de São Paulo, área endêmica para leishmaniose visceral canina, soropositivos para L. (L.) chagasi, de acordo com ELISA indireto, foram divididos em dois grupos com 20 cães assintomáticos e 20 sintomáticos, com pelo menos três sinais da doença. Um grupo de 12 cães saudáveis, provenientes de área não endêmica, soronegativos para Leishmania spp., testados por ELISA indireto e que não apresentaram amplificação do DNA para L. (L.) chagasi, fizeram parte do grupo controle negativo. Após eutanásia dos cães, os fragmentos de baço e fígado foram coletados para a quantificação das citocinas, através de ELISA de captura, e determinação da densidade parasitária por PCR em tempo real. Nos animais infectados, os níveis de TNF- , IL-4 e IL-10, no baço e no fígado, foram superiores aos dos animais do grupo controle. A comparação entre os dois órgãos, nos cães infectados, mostrou que o fígado foi o principal produtor dessas citocinas. O nível de TNF- e a densidade de parasitas, no fígado, foram mais elevados nos cães sintomáticos, quando comparado com os cães...
Canine visceral leishmaniasis is caused by Leishmania (Leishmania) chagasi that is transmitted by phlebotominae. The clinical evolution of this parasitosis depends on a complex interaction between the parasite and the immune response in the host. Infected dogs, the main domestic reservoir of this parasite, may remain asymptomatic or may become symptomatic. The aim of this study was to quantify the TNF-, IL-4, and IL-10 cytokines in spleen and liver extracts from asymptomatic and symptomatic dogs naturally infected with L. (L.) chagasi and to investigate the association with the parasite density in these organs. A total of 40 dogs from the city of Araçatuba, São Paulo state (an endemic area for canine visceral leishmaniasis), all L. (L.) chagasi positive according to indirect ELISA, were divided into two groups, each containing of 20 asymptomatic dogs and 20 symptomatic dogs presenting at least three signs of the disease. A group of 12 healthy dogs from the non endemic area and negative for Leishmania spp, as indicated by indirect ELISA, and PCR negative for L. (L.) chagasi, were used as negative controls. After euthanasia, fragments from the spleen or liver were collected to quantify the cytokines, with ELISA capture assay, and to check parasite density by real time PCR. In infected dogs, the levels of TNF- , IL-4, and IL-10 were higher than in control animals, for the two organs. Cytokine levels in the spleen and liver of infected dogs revealed the liver as the main cytokine-producing organ during infection. The level of TNF- was higher in the liver of symptomatic dogs, where parasite density was higher than in asymptomatic dogs. The levels of IL-4 and IL-10 did not differ between symptomatic and asymptomatic dogs. A weak association between parasite density and IL-10 production was seen in the liver of asymptomatic... (Summary complete electronic access click below)
Canine visceral leishmaniasis is caused by Leishmania (Leishmania) chagasi that is transmitted by phlebotominae. The clinical evolution of this parasitosis depends on a complex interaction between the parasite and the immune response in the host. Infected dogs, the main domestic reservoir of this parasite, may remain asymptomatic or may become symptomatic. The aim of this study was to quantify the TNF-, IL-4, and IL-10 cytokines in spleen and liver extracts from asymptomatic and symptomatic dogs naturally infected with L. (L.) chagasi and to investigate the association with the parasite density in these organs. A total of 40 dogs from the city of Araçatuba, São Paulo state (an endemic area for canine visceral leishmaniasis), all L. (L.) chagasi positive according to indirect ELISA, were divided into two groups, each containing of 20 asymptomatic dogs and 20 symptomatic dogs presenting at least three signs of the disease. A group of 12 healthy dogs from the non endemic area and negative for Leishmania spp, as indicated by indirect ELISA, and PCR negative for L. (L.) chagasi, were used as negative controls. After euthanasia, fragments from the spleen or liver were collected to quantify the cytokines, with ELISA capture assay, and to check parasite density by real time PCR. In infected dogs, the levels of TNF- , IL-4, and IL-10 were higher than in control animals, for the two organs. Cytokine levels in the spleen and liver of infected dogs revealed the liver as the main cytokine-producing organ during infection. The level of TNF- was higher in the liver of symptomatic dogs, where parasite density was higher than in asymptomatic dogs. The levels of IL-4 and IL-10 did not differ between symptomatic and asymptomatic dogs. A weak association between parasite density and IL-10 production was seen in the liver of asymptomatic... (Summary complete electronic access click below)
Descrição
Palavras-chave
Cão, Dionisio Divindade grega, Citocinas, Leishmaniose, Cytokines, Dog, Leishmaniasis, Liver, Spleen, TNF-alfa
Como citar
MICHELIN, Aparecida de Fátima. Níveis de TNF-alfa, IL-4 e IL-10 no baço e no fígado de cães naturalmente infectados por Leishmania (Leishmania) chagasi. 2009. xxii, 68 f. Tese (doutorado) - Universidade Estadual Paulista, Faculdade de Ciências Agrárias e Veterinárias, 2009.