Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/18589
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dc.contributor.authorMachado, Marcus Paulo Ribeiro
dc.contributor.authorRocha, Aletheia Moraes
dc.contributor.authorOliveira, Lucas Felipe de
dc.contributor.authorCuba, Marília Beatriz de
dc.contributor.authorLoss, Igor de Oliveira
dc.contributor.authorCastellano, Lucio Roberto
dc.contributor.authorSilva, Marcus Vinicius
dc.contributor.authorMachado, Juliana Reis
dc.contributor.authorNascentes, Gabriel Antonio Nogueira
dc.contributor.authorPaiva, Luciano Henrique
dc.contributor.authorSavino, Wilson
dc.contributor.authorJunior, Virmondes Rodrigues
dc.contributor.authorBrum, Patricia Chakur
dc.contributor.authorPrado, Vania Ferreira
dc.contributor.authorPrado, Marco Antonio Maximo
dc.contributor.authorSilva, Eliane Lages
dc.contributor.authorMontano, Nicola
dc.contributor.authorRamirez, Luis Eduardo
dc.contributor.authorSilva, Valdo Jose Dias da
dc.date.accessioned2017-04-20T13:10:43Z
dc.date.available2017-04-20T13:10:43Z
dc.date.issued2012
dc.identifier.citationMACHADO, Marcus Paulo Ribeiro; et al. Autonomic nervous system modulation affects the inflammatory immune response in mice with acute Chagas disease. Exp Physiol, v.97. n.11, p 1186–1202, 2012.
dc.identifier.issn0958-0670
dc.identifier.urihttps://www.arca.fiocruz.br/handle/icict/18589
dc.language.isoeng
dc.publisherWiley
dc.rightsrestricted access
dc.subject.otherDoença de Chagas
dc.subject.otherRatos
dc.subject.otherSstema nervoso autônomo
dc.subject.otherResposta imunológica inflamatória
dc.subject.otherFase aguda
dc.titleAutonomic nervous system modulation affects the inflammatory immune response in mice with acute Chagas disease
dc.typeArticle
dc.identifier.doi10.1113/expphysiol.2012.066431
dc.description.abstractenThe aim of the present study was to evaluate the effects of changes to the autonomic nervous system in mice during the acute phase of Chagas disease, which is an infection caused by the parasite Trypanosoma cruzi. The following types of mice were inoculated with T. cruzi (CHG): wild-type (WT) and vesicular acetylcholine transporter knockdown (KDVAChT) C57BL/6j mice; wild-type non-treated (NT) FVB mice; FVB mice treated with pyridostigmine bromide (PYR) or salbutamol (SALB); and β(2)-adrenergic receptor knockout (KOβ2) FVB mice. During infection and at 18-21 days after infection (acute phase), the survival curves, parasitaemia, electrocardiograms, heart rate variability, autonomic tonus and histopathology of the animals were evaluated. Negative control groups were matched for age, genetic background and treatment. The KDVAChT-CHG mice exhibited a significant shift in the electrocardiographic, autonomic and histopathological profiles towards a greater inflammatory immune response that was associated with a reduction in blood and tissue parasitism. In contrast, the CHG-PYR mice manifested reduced myocardial inflammation and lower blood and tissue parasitism. Similar results were observed in CHG-SALB animals. Unexpectedly, the KOβ2-CHG mice exhibited less myocardial inflammation and higher blood and tissue parasitism, which were associated with reduced mortality. These findings could have been due to the increase in vagal tone observed in the KOβ2 mice, which rendered them more similar to the CHG-PYR animals. In conclusion, our results indicate a marked immunomodulatory role for the parasympathetic and sympathetic autonomic nervous systems, which inhibit both the inflammatory immune response and parasite clearance during the acute phase of experimental Chagas heart disease in mice.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal da Paraíba. João Pessoa, PB, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversidade de São Paulo. Escola de Educação Física e Esportes. São Paulo, SP, Brasil.
dc.creator.affilliationUniversity of Western Ontario. Schulich School of Medicine & Dentistry. Robarts Research Institute. Molecular Brain Research Group. Ontario, Canada.
dc.creator.affilliationUniversity of Western Ontario. Schulich School of Medicine & Dentistry. Robarts Research Institute. Molecular Brain Research Group. Ontario, Canada.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.creator.affilliationUniversity of Milan. Department of Clinical Sciences. Internal Medicine II, L. Sacco Hospital. Milano, Italy.
dc.creator.affilliationUniversidade Federal do Triângulo Mineiro. Instituto de Ciências Biológicas. Uberaba, MG, Brasil.
dc.subject.enAutonomic nervous system
dc.subject.eninflammatory immune response
dc.subject.enmice
dc.subject.enChagas Disease
dc.subject.enacute phase
dc.identifier.eissn1469-445X
Appears in Collections:IOC - Artigos de Periódicos

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