Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.

Detalhes bibliográficos
Autor(a) principal: Avelar, Renato Sathler
Data de Publicação: 2008
Outros Autores: Avelar, Danielle Marchetti Vitelli, Massara, Rodrigo Lima, Lana, Marta de, Dias, João Carlos Pinto, Carvalho, Andréa Teixeira de, Santos, Silvana Maria Elói, Martins Filho, Olindo Assis
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFOP
Texto Completo: http://www.repositorio.ufop.br/handle/123456789/3966
https://doi.org/10.1016/j.micinf.2007.10.009
Resumo: Pro-inflammatory immune response is usually associated with Chagas disease pathogenesis, but is also relevant to treatment effectiveness. Cross-sectional studies have suggested that this activated state may persist for years after therapeutic intervention. However, short-term longitudinal investigation has suggested that the Benznidazole treatment (Bz-treatment) leads to decreased immunological activation. In order to elucidate this issue, we performed a longitudinal study to evaluate the immunological status following Bz-treatment during early indeterminate Chagas disease. Our results demonstrated that Bz-treatment led to higher activation status of circulating monocytes but was negatively associated with the number of IL-12þCD14þ cells. Moreover, Bz-treatment triggered a high frequency of circulating CD3_CD16þCD56_ NK cells, in addition to elevated activation status associated with a type 1-modulated cytokine pattern. Bz-treatment induced substantial T and B-cell activation status associated with an overall IL-10 modulated type 1 cytokine profile. In summary, these findings provide new information regarding immune activation status following the etiological treatment of Chagas disease. These results suggest that in addition to the increased number of activated leukocytes in the peripheral blood, Bz-treatment may also involve a qualitative change in their functional capacity that drives their activation state toward a modulated cytokine profile. These changes may account for the benefits of etiological treatment of Chagas disease.
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spelling Avelar, Renato SathlerAvelar, Danielle Marchetti VitelliMassara, Rodrigo LimaLana, Marta deDias, João Carlos PintoCarvalho, Andréa Teixeira deSantos, Silvana Maria ElóiMartins Filho, Olindo Assis2014-11-19T15:40:49Z2014-11-19T15:40:49Z2008AVELAR, R. S. et al. Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern. Microbes and Infection, v. 10, p. 103-113, 2008. Disponível em: <http://www.sciencedirect.com/science/article/pii/S1286457907003310>. Acesso em: 28 ago. 2014.1286-4579http://www.repositorio.ufop.br/handle/123456789/3966https://doi.org/10.1016/j.micinf.2007.10.009Pro-inflammatory immune response is usually associated with Chagas disease pathogenesis, but is also relevant to treatment effectiveness. Cross-sectional studies have suggested that this activated state may persist for years after therapeutic intervention. However, short-term longitudinal investigation has suggested that the Benznidazole treatment (Bz-treatment) leads to decreased immunological activation. In order to elucidate this issue, we performed a longitudinal study to evaluate the immunological status following Bz-treatment during early indeterminate Chagas disease. Our results demonstrated that Bz-treatment led to higher activation status of circulating monocytes but was negatively associated with the number of IL-12þCD14þ cells. Moreover, Bz-treatment triggered a high frequency of circulating CD3_CD16þCD56_ NK cells, in addition to elevated activation status associated with a type 1-modulated cytokine pattern. Bz-treatment induced substantial T and B-cell activation status associated with an overall IL-10 modulated type 1 cytokine profile. In summary, these findings provide new information regarding immune activation status following the etiological treatment of Chagas disease. These results suggest that in addition to the increased number of activated leukocytes in the peripheral blood, Bz-treatment may also involve a qualitative change in their functional capacity that drives their activation state toward a modulated cytokine profile. These changes may account for the benefits of etiological treatment of Chagas disease.Chagas diseaseBenznidazoleImmune responseCytokinesLeukocytes subsetsEtiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleO periódico Microbes and Infection concede permissão para depósito deste artigo no Repositório Institucional da UFOP. 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dc.title.pt_BR.fl_str_mv Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
title Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
spellingShingle Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
Avelar, Renato Sathler
Chagas disease
Benznidazole
Immune response
Cytokines
Leukocytes subsets
title_short Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
title_full Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
title_fullStr Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
title_full_unstemmed Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
title_sort Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern.
author Avelar, Renato Sathler
author_facet Avelar, Renato Sathler
Avelar, Danielle Marchetti Vitelli
Massara, Rodrigo Lima
Lana, Marta de
Dias, João Carlos Pinto
Carvalho, Andréa Teixeira de
Santos, Silvana Maria Elói
Martins Filho, Olindo Assis
author_role author
author2 Avelar, Danielle Marchetti Vitelli
Massara, Rodrigo Lima
Lana, Marta de
Dias, João Carlos Pinto
Carvalho, Andréa Teixeira de
Santos, Silvana Maria Elói
Martins Filho, Olindo Assis
author2_role author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Avelar, Renato Sathler
Avelar, Danielle Marchetti Vitelli
Massara, Rodrigo Lima
Lana, Marta de
Dias, João Carlos Pinto
Carvalho, Andréa Teixeira de
Santos, Silvana Maria Elói
Martins Filho, Olindo Assis
dc.subject.por.fl_str_mv Chagas disease
Benznidazole
Immune response
Cytokines
Leukocytes subsets
topic Chagas disease
Benznidazole
Immune response
Cytokines
Leukocytes subsets
description Pro-inflammatory immune response is usually associated with Chagas disease pathogenesis, but is also relevant to treatment effectiveness. Cross-sectional studies have suggested that this activated state may persist for years after therapeutic intervention. However, short-term longitudinal investigation has suggested that the Benznidazole treatment (Bz-treatment) leads to decreased immunological activation. In order to elucidate this issue, we performed a longitudinal study to evaluate the immunological status following Bz-treatment during early indeterminate Chagas disease. Our results demonstrated that Bz-treatment led to higher activation status of circulating monocytes but was negatively associated with the number of IL-12þCD14þ cells. Moreover, Bz-treatment triggered a high frequency of circulating CD3_CD16þCD56_ NK cells, in addition to elevated activation status associated with a type 1-modulated cytokine pattern. Bz-treatment induced substantial T and B-cell activation status associated with an overall IL-10 modulated type 1 cytokine profile. In summary, these findings provide new information regarding immune activation status following the etiological treatment of Chagas disease. These results suggest that in addition to the increased number of activated leukocytes in the peripheral blood, Bz-treatment may also involve a qualitative change in their functional capacity that drives their activation state toward a modulated cytokine profile. These changes may account for the benefits of etiological treatment of Chagas disease.
publishDate 2008
dc.date.issued.fl_str_mv 2008
dc.date.accessioned.fl_str_mv 2014-11-19T15:40:49Z
dc.date.available.fl_str_mv 2014-11-19T15:40:49Z
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dc.identifier.citation.fl_str_mv AVELAR, R. S. et al. Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern. Microbes and Infection, v. 10, p. 103-113, 2008. Disponível em: <http://www.sciencedirect.com/science/article/pii/S1286457907003310>. Acesso em: 28 ago. 2014.
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dc.identifier.issn.none.fl_str_mv 1286-4579
dc.identifier.doi.none.fl_str_mv https://doi.org/10.1016/j.micinf.2007.10.009
identifier_str_mv AVELAR, R. S. et al. Etiological treatment during early chronic indeterminate Chagas disease incites an activated status on innate and adaptive immunity associated with a type 1-modulated cytokine pattern. Microbes and Infection, v. 10, p. 103-113, 2008. Disponível em: <http://www.sciencedirect.com/science/article/pii/S1286457907003310>. Acesso em: 28 ago. 2014.
1286-4579
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https://doi.org/10.1016/j.micinf.2007.10.009
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