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Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection
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 ca...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Associação Brasileira de Divulgação Científica
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5886554/ https://www.ncbi.nlm.nih.gov/pubmed/29590257 http://dx.doi.org/10.1590/1414-431X20186690 |
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author | Silva, M.C. Azevedo, M.A. Figueiredo, V.P. Moura, M.R. Coelho, D. Martinelli, P.M. Machado, R.P. Alzamora, A.C. Talvani, A. |
author_facet | Silva, M.C. Azevedo, M.A. Figueiredo, V.P. Moura, M.R. Coelho, D. Martinelli, P.M. Machado, R.P. Alzamora, A.C. Talvani, A. |
author_sort | Silva, M.C. |
collection | PubMed |
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. |
format | Online Article Text |
id | pubmed-5886554 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Associação Brasileira de Divulgação Científica |
record_format | MEDLINE/PubMed |
spelling | pubmed-58865542018-04-06 Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection Silva, M.C. Azevedo, M.A. Figueiredo, V.P. Moura, M.R. Coelho, D. Martinelli, P.M. Machado, R.P. Alzamora, A.C. Talvani, A. Braz J Med Biol Res Research Articles 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. Associação Brasileira de Divulgação Científica 2018-03-26 /pmc/articles/PMC5886554/ /pubmed/29590257 http://dx.doi.org/10.1590/1414-431X20186690 Text en https://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Silva, M.C. Azevedo, M.A. Figueiredo, V.P. Moura, M.R. Coelho, D. Martinelli, P.M. Machado, R.P. Alzamora, A.C. Talvani, A. Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection |
title | 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_short | 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 |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5886554/ https://www.ncbi.nlm.nih.gov/pubmed/29590257 http://dx.doi.org/10.1590/1414-431X20186690 |
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