Stress related hormonal circuitry in chagas disease

Autores
Lepletier, Ailin; Villar, Silvina Raquel; Perez, Ana Rosa; Morrot, Alexandre; Savino, Wilson
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
During stressful processes, for example infectious diseases, neuroendocrine and immune networks act multi-directionally facilitating the host response. However in exacerbated settings, this homeostatic mechanism may be lost. Recent findings unravelled an imbalance of the immunoneuroendocrine network during Chagas disease, the infection caused by the protozoan Trypanosoma cruzi. During the acute immune response against T. cruzi, inflammatory and neuroendocrine responses become dysregulated with harmful effects for the host. One target organ is the thymus. In acutely-infected mice, it undergoes a severe atrophy, with massive depletion of immature double positive CD4+CD8+ (DP) thymocytes, which seems to be linked to a systemic and intrathymic cytokine/hormonal imbalance, involving TNF-α, glucocorticoids and prolactin. In addition, there is an abnormal export of potentially autoreactive DP cells to the periphery of the immune system, which is apparently regulated by the prolactin levels. Furthermore, TNF-α is able to differentially modulate the hypothalamus-pituitary-adrenal (HPA) axis: while having stimulatory effects at the HP unit at the adrenal it is inhibitory. Interestingly, chronically infected humans with chagasic myocardiopathy also showed alterations in HPA axis. Understanding of how T. cruzi infection lead to neuroendocrine immune-associated disturbances will provide important clues to better dissect the mechanisms underlying the pathophysiology of Chagas disease.
Fil: Lepletier, Ailin. Instituto Oswaldo Cruz; Brasil
Fil: Villar, Silvina Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Perez, Ana Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Morrot, Alexandre. Universidade Federal do Rio de Janeiro; Brasil
Fil: Savino, Wilson. Instituto Oswaldo Cruz; Brasil
Materia
CHAGAS DISEASE
DOUBLE POSITIVE T CELLS
HORMONAL CIRCUITRY
LYMPH NODES
THYMUS ATROPHY
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/95259
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Stress related hormonal circuitry in chagas diseaseLepletier, AilinVillar, Silvina RaquelPerez, Ana RosaMorrot, AlexandreSavino, WilsonCHAGAS DISEASEDOUBLE POSITIVE T CELLSHORMONAL CIRCUITRYLYMPH NODESTHYMUS ATROPHYhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3During stressful processes, for example infectious diseases, neuroendocrine and immune networks act multi-directionally facilitating the host response. However in exacerbated settings, this homeostatic mechanism may be lost. Recent findings unravelled an imbalance of the immunoneuroendocrine network during Chagas disease, the infection caused by the protozoan Trypanosoma cruzi. During the acute immune response against T. cruzi, inflammatory and neuroendocrine responses become dysregulated with harmful effects for the host. One target organ is the thymus. In acutely-infected mice, it undergoes a severe atrophy, with massive depletion of immature double positive CD4+CD8+ (DP) thymocytes, which seems to be linked to a systemic and intrathymic cytokine/hormonal imbalance, involving TNF-α, glucocorticoids and prolactin. In addition, there is an abnormal export of potentially autoreactive DP cells to the periphery of the immune system, which is apparently regulated by the prolactin levels. Furthermore, TNF-α is able to differentially modulate the hypothalamus-pituitary-adrenal (HPA) axis: while having stimulatory effects at the HP unit at the adrenal it is inhibitory. Interestingly, chronically infected humans with chagasic myocardiopathy also showed alterations in HPA axis. Understanding of how T. cruzi infection lead to neuroendocrine immune-associated disturbances will provide important clues to better dissect the mechanisms underlying the pathophysiology of Chagas disease.Fil: Lepletier, Ailin. Instituto Oswaldo Cruz; BrasilFil: Villar, Silvina Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Perez, Ana Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Morrot, Alexandre. Universidade Federal do Rio de Janeiro; BrasilFil: Savino, Wilson. Instituto Oswaldo Cruz; BrasilIOS Press2014-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/95259Lepletier, Ailin; Villar, Silvina Raquel; Perez, Ana Rosa; Morrot, Alexandre; Savino, Wilson; Stress related hormonal circuitry in chagas disease; IOS Press; Advances in Neuroimmune Biology; 5; 2; 7-2014; 91-981878-948X1878-9498CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://content.iospress.com/articles/advances-in-neuroimmune-biology/nib140094info:eu-repo/semantics/altIdentifier/doi/10.3233/NIB-140094info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:18:22Zoai:ri.conicet.gov.ar:11336/95259instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 12:18:22.771CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Stress related hormonal circuitry in chagas disease
title Stress related hormonal circuitry in chagas disease
spellingShingle Stress related hormonal circuitry in chagas disease
Lepletier, Ailin
CHAGAS DISEASE
DOUBLE POSITIVE T CELLS
HORMONAL CIRCUITRY
LYMPH NODES
THYMUS ATROPHY
title_short Stress related hormonal circuitry in chagas disease
title_full Stress related hormonal circuitry in chagas disease
title_fullStr Stress related hormonal circuitry in chagas disease
title_full_unstemmed Stress related hormonal circuitry in chagas disease
title_sort Stress related hormonal circuitry in chagas disease
dc.creator.none.fl_str_mv Lepletier, Ailin
Villar, Silvina Raquel
Perez, Ana Rosa
Morrot, Alexandre
Savino, Wilson
author Lepletier, Ailin
author_facet Lepletier, Ailin
Villar, Silvina Raquel
Perez, Ana Rosa
Morrot, Alexandre
Savino, Wilson
author_role author
author2 Villar, Silvina Raquel
Perez, Ana Rosa
Morrot, Alexandre
Savino, Wilson
author2_role author
author
author
author
dc.subject.none.fl_str_mv CHAGAS DISEASE
DOUBLE POSITIVE T CELLS
HORMONAL CIRCUITRY
LYMPH NODES
THYMUS ATROPHY
topic CHAGAS DISEASE
DOUBLE POSITIVE T CELLS
HORMONAL CIRCUITRY
LYMPH NODES
THYMUS ATROPHY
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv During stressful processes, for example infectious diseases, neuroendocrine and immune networks act multi-directionally facilitating the host response. However in exacerbated settings, this homeostatic mechanism may be lost. Recent findings unravelled an imbalance of the immunoneuroendocrine network during Chagas disease, the infection caused by the protozoan Trypanosoma cruzi. During the acute immune response against T. cruzi, inflammatory and neuroendocrine responses become dysregulated with harmful effects for the host. One target organ is the thymus. In acutely-infected mice, it undergoes a severe atrophy, with massive depletion of immature double positive CD4+CD8+ (DP) thymocytes, which seems to be linked to a systemic and intrathymic cytokine/hormonal imbalance, involving TNF-α, glucocorticoids and prolactin. In addition, there is an abnormal export of potentially autoreactive DP cells to the periphery of the immune system, which is apparently regulated by the prolactin levels. Furthermore, TNF-α is able to differentially modulate the hypothalamus-pituitary-adrenal (HPA) axis: while having stimulatory effects at the HP unit at the adrenal it is inhibitory. Interestingly, chronically infected humans with chagasic myocardiopathy also showed alterations in HPA axis. Understanding of how T. cruzi infection lead to neuroendocrine immune-associated disturbances will provide important clues to better dissect the mechanisms underlying the pathophysiology of Chagas disease.
Fil: Lepletier, Ailin. Instituto Oswaldo Cruz; Brasil
Fil: Villar, Silvina Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Perez, Ana Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Morrot, Alexandre. Universidade Federal do Rio de Janeiro; Brasil
Fil: Savino, Wilson. Instituto Oswaldo Cruz; Brasil
description During stressful processes, for example infectious diseases, neuroendocrine and immune networks act multi-directionally facilitating the host response. However in exacerbated settings, this homeostatic mechanism may be lost. Recent findings unravelled an imbalance of the immunoneuroendocrine network during Chagas disease, the infection caused by the protozoan Trypanosoma cruzi. During the acute immune response against T. cruzi, inflammatory and neuroendocrine responses become dysregulated with harmful effects for the host. One target organ is the thymus. In acutely-infected mice, it undergoes a severe atrophy, with massive depletion of immature double positive CD4+CD8+ (DP) thymocytes, which seems to be linked to a systemic and intrathymic cytokine/hormonal imbalance, involving TNF-α, glucocorticoids and prolactin. In addition, there is an abnormal export of potentially autoreactive DP cells to the periphery of the immune system, which is apparently regulated by the prolactin levels. Furthermore, TNF-α is able to differentially modulate the hypothalamus-pituitary-adrenal (HPA) axis: while having stimulatory effects at the HP unit at the adrenal it is inhibitory. Interestingly, chronically infected humans with chagasic myocardiopathy also showed alterations in HPA axis. Understanding of how T. cruzi infection lead to neuroendocrine immune-associated disturbances will provide important clues to better dissect the mechanisms underlying the pathophysiology of Chagas disease.
publishDate 2014
dc.date.none.fl_str_mv 2014-07
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/95259
Lepletier, Ailin; Villar, Silvina Raquel; Perez, Ana Rosa; Morrot, Alexandre; Savino, Wilson; Stress related hormonal circuitry in chagas disease; IOS Press; Advances in Neuroimmune Biology; 5; 2; 7-2014; 91-98
1878-948X
1878-9498
CONICET Digital
CONICET
url http://hdl.handle.net/11336/95259
identifier_str_mv Lepletier, Ailin; Villar, Silvina Raquel; Perez, Ana Rosa; Morrot, Alexandre; Savino, Wilson; Stress related hormonal circuitry in chagas disease; IOS Press; Advances in Neuroimmune Biology; 5; 2; 7-2014; 91-98
1878-948X
1878-9498
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://content.iospress.com/articles/advances-in-neuroimmune-biology/nib140094
info:eu-repo/semantics/altIdentifier/doi/10.3233/NIB-140094
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv IOS Press
publisher.none.fl_str_mv IOS Press
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.982451

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