Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFMG |
Texto Completo: | http://hdl.handle.net/1843/44332 |
Resumo: | Trypanosoma cruzi triggers a progressive inflammatory response affecting cardiovascular functions in humans and experimental models. Angiotensin II, a key effector of the renin-angiotensin system, plays roles in mediating hypertension, heart failure, and inflammatory responses. T. cruzi and AngII can induce inflammatory responses by releasing inflammatory mediators. The aim of this study was to evaluate systemic AngII, tumor necrosis factor (TNF), and CX3CL1 mediators in a two-kidney one-clip (2K1C) renovascular hypertension model using Wistar rats infected with T. cruzi. Our data showed an increase in serum AngII in uninfected and T. cruzi-infected rats 1 week after 2K1C surgery compared to non-2K1C (Sham) animals. The baseline systolic blood pressure was higher in both uninfected and infected 2K1C rats. Despite no difference in circulating parasites in the acute phase of infection, elevated serum TNF and CX3CL1 were observed at 8 weeks post-infection in 2K1C rats in association with higher cardiac inflammatory infiltration. In summary, AngII-induced hypertension associated with T. cruzi infection may act synergistically to increase TNF and CX3CL1 in the 2K1C rat model, thereby intensifying cardiac inflammatory infiltration and worsening the underlying inflammation triggered by this protozoan. |
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2022-08-17T19:57:30Z2022-08-17T19:57:30Z201810.1590/1414-431x201866901414-431Xhttp://hdl.handle.net/1843/44332Trypanosoma cruzi triggers a progressive inflammatory response affecting cardiovascular functions in humans and experimental models. Angiotensin II, a key effector of the renin-angiotensin system, plays roles in mediating hypertension, heart failure, and inflammatory responses. T. cruzi and AngII can induce inflammatory responses by releasing inflammatory mediators. The aim of this study was to evaluate systemic AngII, tumor necrosis factor (TNF), and CX3CL1 mediators in a two-kidney one-clip (2K1C) renovascular hypertension model using Wistar rats infected with T. cruzi. Our data showed an increase in serum AngII in uninfected and T. cruzi-infected rats 1 week after 2K1C surgery compared to non-2K1C (Sham) animals. The baseline systolic blood pressure was higher in both uninfected and infected 2K1C rats. Despite no difference in circulating parasites in the acute phase of infection, elevated serum TNF and CX3CL1 were observed at 8 weeks post-infection in 2K1C rats in association with higher cardiac inflammatory infiltration. In summary, AngII-induced hypertension associated with T. cruzi infection may act synergistically to increase TNF and CX3CL1 in the 2K1C rat model, thereby intensifying cardiac inflammatory infiltration and worsening the underlying inflammation triggered by this protozoan.Trypanosoma cruzi desencadeia uma resposta inflamatória progressiva afetando funções cardiovasculares em humanos e modelos experimentais. A angiotensina II, um efetor chave do sistema renina-angiotensina, desempenha papéis na mediação da hipertensão, insuficiência cardíaca e respostas inflamatórias. T. cruzi e AngII podem induzir respostas inflamatórias pela liberação de mediadores inflamatórios. O objetivo deste estudo foi avaliar AngII sistêmica, fator de necrose tumoral (TNF) e mediadores CX3CL1 em um modelo de hipertensão renovascular de dois rins (2R1C) usando ratos Wistar infectados com T. cruzi. Nossos dados mostraram um aumento na AngII sérica em ratos não infectados e infectados por T. cruzi 1 semana após a cirurgia 2R1C em comparação com animais não 2R1C (Sham). A pressão arterial sistólica basal foi maior em ratos 2R1C não infectados e infectados. Apesar de não haver diferença nos parasitas circulantes na fase aguda da infecção, TNF e CX3CL1 séricos elevados foram observados 8 semanas após a infecção em ratos 2R1C em associação com maior infiltrado inflamatório cardíaco. Em resumo, a hipertensão induzida por AngII associada à infecção por T. cruzi pode atuar sinergicamente para aumentar TNF e CX3CL1 no modelo de rato 2R1C, intensificando assim a infiltração inflamatória cardíaca e piorando a inflamação subjacente desencadeada por este protozoário.engUniversidade Federal de Minas GeraisUFMGBrasilICB - DEPARTAMENTO DE MORFOLOGIABrazilian journal of medical and biological researchTrypanosoma cruziHipertensãoFator de Necrose TumoralCX3CL1Inflamação CardíacaRenovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infectionHipertensão renovascular aumenta TNF e CX3CL1 séricos em infecção experimental por Trypanosoma cruziinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttps://www.scielo.br/j/bjmbr/a/BGdyfdPfHcDk3FxrL7cf8ND/?lang=enM. C. SilvaM. A. AzevedoVivian Paulino FigueiredoM. R. Moura JuniorD. Coelho JuniorP. M. MartinelliR. P. MachadoA.C. AlzamoraAndré Talvaniapplication/pdfinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMGLICENSELicense.txtLicense.txttext/plain; charset=utf-82042https://repositorio.ufmg.br/bitstream/1843/44332/1/License.txtfa505098d172de0bc8864fc1287ffe22MD51ORIGINAL2018_Renovascular hypertension increases serum tnf and cx3cl1 in experimental trypanosoma cruzi infection.pdf2018_Renovascular hypertension increases serum tnf and cx3cl1 in experimental trypanosoma cruzi infection.pdfapplication/pdf2345952https://repositorio.ufmg.br/bitstream/1843/44332/2/2018_Renovascular%20hypertension%20increases%20serum%20tnf%20and%20cx3cl1%20in%20experimental%20trypanosoma%20cruzi%20infection.pdf4caca81539b48425b64741cd4d7a92b2MD521843/443322022-08-17 16:57:30.132oai:repositorio.ufmg.br:1843/44332TElDRU7vv71BIERFIERJU1RSSUJVSe+/ve+/vU8gTu+/vU8tRVhDTFVTSVZBIERPIFJFUE9TSVTvv71SSU8gSU5TVElUVUNJT05BTCBEQSBVRk1HCiAKCkNvbSBhIGFwcmVzZW50Ye+/ve+/vW8gZGVzdGEgbGljZW7vv71hLCB2b2Pvv70gKG8gYXV0b3IgKGVzKSBvdSBvIHRpdHVsYXIgZG9zIGRpcmVpdG9zIGRlIGF1dG9yKSBjb25jZWRlIGFvIFJlcG9zaXTvv71yaW8gSW5zdGl0dWNpb25hbCBkYSBVRk1HIChSSS1VRk1HKSBvIGRpcmVpdG8gbu+/vW8gZXhjbHVzaXZvIGUgaXJyZXZvZ++/vXZlbCBkZSByZXByb2R1emlyIGUvb3UgZGlzdHJpYnVpciBhIHN1YSBwdWJsaWNh77+977+9byAoaW5jbHVpbmRvIG8gcmVzdW1vKSBwb3IgdG9kbyBvIG11bmRvIG5vIGZvcm1hdG8gaW1wcmVzc28gZSBlbGV0cu+/vW5pY28gZSBlbSBxdWFscXVlciBtZWlvLCBpbmNsdWluZG8gb3MgZm9ybWF0b3Mg77+9dWRpbyBvdSB277+9ZGVvLgoKVm9j77+9IGRlY2xhcmEgcXVlIGNvbmhlY2UgYSBwb2zvv710aWNhIGRlIGNvcHlyaWdodCBkYSBlZGl0b3JhIGRvIHNldSBkb2N1bWVudG8gZSBxdWUgY29uaGVjZSBlIGFjZWl0YSBhcyBEaXJldHJpemVzIGRvIFJJLVVGTUcuCgpWb2Pvv70gY29uY29yZGEgcXVlIG8gUmVwb3NpdO+/vXJpbyBJbnN0aXR1Y2lvbmFsIGRhIFVGTUcgcG9kZSwgc2VtIGFsdGVyYXIgbyBjb250Ze+/vWRvLCB0cmFuc3BvciBhIHN1YSBwdWJsaWNh77+977+9byBwYXJhIHF1YWxxdWVyIG1laW8gb3UgZm9ybWF0byBwYXJhIGZpbnMgZGUgcHJlc2VydmHvv73vv71vLgoKVm9j77+9IHRhbWLvv71tIGNvbmNvcmRhIHF1ZSBvIFJlcG9zaXTvv71yaW8gSW5zdGl0dWNpb25hbCBkYSBVRk1HIHBvZGUgbWFudGVyIG1haXMgZGUgdW1hIGPvv71waWEgZGUgc3VhIHB1YmxpY2Hvv73vv71vIHBhcmEgZmlucyBkZSBzZWd1cmFu77+9YSwgYmFjay11cCBlIHByZXNlcnZh77+977+9by4KClZvY++/vSBkZWNsYXJhIHF1ZSBhIHN1YSBwdWJsaWNh77+977+9byDvv70gb3JpZ2luYWwgZSBxdWUgdm9j77+9IHRlbSBvIHBvZGVyIGRlIGNvbmNlZGVyIG9zIGRpcmVpdG9zIGNvbnRpZG9zIG5lc3RhIGxpY2Vu77+9YS4gVm9j77+9IHRhbWLvv71tIGRlY2xhcmEgcXVlIG8gZGVw77+9c2l0byBkZSBzdWEgcHVibGljYe+/ve+/vW8gbu+/vW8sIHF1ZSBzZWphIGRlIHNldSBjb25oZWNpbWVudG8sIGluZnJpbmdlIGRpcmVpdG9zIGF1dG9yYWlzIGRlIG5pbmd177+9bS4KCkNhc28gYSBzdWEgcHVibGljYe+/ve+/vW8gY29udGVuaGEgbWF0ZXJpYWwgcXVlIHZvY++/vSBu77+9byBwb3NzdWkgYSB0aXR1bGFyaWRhZGUgZG9zIGRpcmVpdG9zIGF1dG9yYWlzLCB2b2Pvv70gZGVjbGFyYSBxdWUgb2J0ZXZlIGEgcGVybWlzc++/vW8gaXJyZXN0cml0YSBkbyBkZXRlbnRvciBkb3MgZGlyZWl0b3MgYXV0b3JhaXMgcGFyYSBjb25jZWRlciBhbyBSZXBvc2l077+9cmlvIEluc3RpdHVjaW9uYWwgZGEgVUZNRyBvcyBkaXJlaXRvcyBhcHJlc2VudGFkb3MgbmVzdGEgbGljZW7vv71hLCBlIHF1ZSBlc3NlIG1hdGVyaWFsIGRlIHByb3ByaWVkYWRlIGRlIHRlcmNlaXJvcyBlc3Tvv70gY2xhcmFtZW50ZSBpZGVudGlmaWNhZG8gZSByZWNvbmhlY2lkbyBubyB0ZXh0byBvdSBubyBjb250Ze+/vWRvIGRhIHB1YmxpY2Hvv73vv71vIG9yYSBkZXBvc2l0YWRhLgoKQ0FTTyBBIFBVQkxJQ0Hvv73vv71PIE9SQSBERVBPU0lUQURBIFRFTkhBIFNJRE8gUkVTVUxUQURPIERFIFVNIFBBVFJPQ++/vU5JTyBPVSBBUE9JTyBERSBVTUEgQUfvv71OQ0lBIERFIEZPTUVOVE8gT1UgT1VUUk8gT1JHQU5JU01PLCBWT0Pvv70gREVDTEFSQSBRVUUgUkVTUEVJVE9VIFRPRE9TIEUgUVVBSVNRVUVSIERJUkVJVE9TIERFIFJFVklT77+9TyBDT01PIFRBTULvv71NIEFTIERFTUFJUyBPQlJJR0Hvv73vv71FUyBFWElHSURBUyBQT1IgQ09OVFJBVE8gT1UgQUNPUkRPLgoKTyBSZXBvc2l077+9cmlvIEluc3RpdHVjaW9uYWwgZGEgVUZNRyBzZSBjb21wcm9tZXRlIGEgaWRlbnRpZmljYXIgY2xhcmFtZW50ZSBvIHNldSBub21lKHMpIG91IG8ocykgbm9tZXMocykgZG8ocykgZGV0ZW50b3IoZXMpIGRvcyBkaXJlaXRvcyBhdXRvcmFpcyBkYSBwdWJsaWNh77+977+9bywgZSBu77+9byBmYXLvv70gcXVhbHF1ZXIgYWx0ZXJh77+977+9bywgYWzvv71tIGRhcXVlbGFzIGNvbmNlZGlkYXMgcG9yIGVzdGEgbGljZW7vv71hLgo=Repositório de PublicaçõesPUBhttps://repositorio.ufmg.br/oaiopendoar:2022-08-17T19:57:30Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)false |
dc.title.pt_BR.fl_str_mv |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
dc.title.alternative.pt_BR.fl_str_mv |
Hipertensão renovascular aumenta TNF e CX3CL1 séricos em infecção experimental por Trypanosoma cruzi |
title |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
spellingShingle |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection M. C. Silva Trypanosoma cruzi Hipertensão Fator de Necrose Tumoral CX3CL1 Inflamação Cardíaca |
title_short |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
title_full |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
title_fullStr |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
title_full_unstemmed |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
title_sort |
Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
author |
M. C. Silva |
author_facet |
M. C. Silva M. A. Azevedo Vivian Paulino Figueiredo M. R. Moura Junior D. Coelho Junior P. M. Martinelli R. P. Machado A.C. Alzamora André Talvani |
author_role |
author |
author2 |
M. A. Azevedo Vivian Paulino Figueiredo M. R. Moura Junior D. Coelho Junior P. M. Martinelli R. P. Machado A.C. Alzamora André Talvani |
author2_role |
author author author author author author author author |
dc.contributor.author.fl_str_mv |
M. C. Silva M. A. Azevedo Vivian Paulino Figueiredo M. R. Moura Junior D. Coelho Junior P. M. Martinelli R. P. Machado A.C. Alzamora André Talvani |
dc.subject.other.pt_BR.fl_str_mv |
Trypanosoma cruzi Hipertensão Fator de Necrose Tumoral CX3CL1 Inflamação Cardíaca |
topic |
Trypanosoma cruzi Hipertensão Fator de Necrose Tumoral CX3CL1 Inflamação Cardíaca |
description |
Trypanosoma cruzi triggers a progressive inflammatory response affecting cardiovascular functions in humans and experimental models. Angiotensin II, a key effector of the renin-angiotensin system, plays roles in mediating hypertension, heart failure, and inflammatory responses. T. cruzi and AngII can induce inflammatory responses by releasing inflammatory mediators. The aim of this study was to evaluate systemic AngII, tumor necrosis factor (TNF), and CX3CL1 mediators in a two-kidney one-clip (2K1C) renovascular hypertension model using Wistar rats infected with T. cruzi. Our data showed an increase in serum AngII in uninfected and T. cruzi-infected rats 1 week after 2K1C surgery compared to non-2K1C (Sham) animals. The baseline systolic blood pressure was higher in both uninfected and infected 2K1C rats. Despite no difference in circulating parasites in the acute phase of infection, elevated serum TNF and CX3CL1 were observed at 8 weeks post-infection in 2K1C rats in association with higher cardiac inflammatory infiltration. In summary, AngII-induced hypertension associated with T. cruzi infection may act synergistically to increase TNF and CX3CL1 in the 2K1C rat model, thereby intensifying cardiac inflammatory infiltration and worsening the underlying inflammation triggered by this protozoan. |
publishDate |
2018 |
dc.date.issued.fl_str_mv |
2018 |
dc.date.accessioned.fl_str_mv |
2022-08-17T19:57:30Z |
dc.date.available.fl_str_mv |
2022-08-17T19:57:30Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/1843/44332 |
dc.identifier.doi.pt_BR.fl_str_mv |
10.1590/1414-431x20186690 |
dc.identifier.issn.pt_BR.fl_str_mv |
1414-431X |
identifier_str_mv |
10.1590/1414-431x20186690 1414-431X |
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http://hdl.handle.net/1843/44332 |
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eng |
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eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Brazilian journal of medical and biological research |
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info:eu-repo/semantics/openAccess |
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openAccess |
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Universidade Federal de Minas Gerais |
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UFMG |
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Brasil |
dc.publisher.department.fl_str_mv |
ICB - DEPARTAMENTO DE MORFOLOGIA |
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Universidade Federal de Minas Gerais |
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reponame:Repositório Institucional da UFMG instname:Universidade Federal de Minas Gerais (UFMG) instacron:UFMG |
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