Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy

Detalhes bibliográficos
Autor(a) principal: Martins, Sílvia
Data de Publicação: 2023
Outros Autores: António, Natália, Carvalheiro, Tiago, Laranjeira, Paula, Rodrigues, Ricardo, Gonçalves, Lino, Tomaz, Cândida, Paiva, Artur
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
Texto Completo: https://hdl.handle.net/10316/111225
https://doi.org/10.1186/s12872-023-03109-x
Resumo: Background T cells have been implicated in the development and progression of inflammatory processes in chronic heart failure (CHF). Cardiac resynchronization therapy (CRT) has beneficial effects on symptoms and cardiac remodeling in CHF. However, its impact on the inflammatory immune response remains controversial. We aimed to study the impact of CRT on T cells in heart failure (HF) patients. Methods Thirty-nine HF patients were evaluated before CRT (T0) and six months later (T6). Quantification of T cells, their subsets, and their functional characterization, after in vitro stimulation, were evaluated by flow cytometry. Results T regulatory (Treg) cells were decreased in CHF patients (healthy group (HG): 1.08 ± 0.50 versus (heart failure patients (HFP)-T0: 0.69 ± 0.40, P = 0.022) and remaining diminished after CRT (HFP-T6: 0.61 ± 0.29, P = 0.003). Responders (R) to CRT presented a higher frequency of T cytotoxic (Tc) cells producing IL-2 at T0 compared with non-responders (NR) (R: 36.52 ± 12.55 versus NR: 24.71 ± 11.66, P = 0.006). After CRT, HF patients presented a higher percentage of Tc cells expressing TNF-α and IFN-γ (HG: 44.50 ± 16.62 versus R: 61.47 ± 20.54, P = 0.014; and HG: 40.62 ± 15.36 versus R: 52.39 ± 18.66, P = 0.049, respectively). Conclusion The dynamic of different functional T cell subpopulations is significantly altered in CHF, which results in an exacerbated pro-inflammatory response. Even after CRT, it seems that the inflammatory condition underlying CHF continues to evolve with the progression of the disease. This could be due, at least in part, to the inability to restore Treg cells levels.
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spelling Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapyChronic heart failureCardiac resynchronization TherapyImmune responseT cellscytokines profileHumansT-Lymphocytes, RegulatoryProspective StudiesHeartChronic DiseaseTreatment OutcomeCardiac Resynchronization TherapyHeart FailureBackground T cells have been implicated in the development and progression of inflammatory processes in chronic heart failure (CHF). Cardiac resynchronization therapy (CRT) has beneficial effects on symptoms and cardiac remodeling in CHF. However, its impact on the inflammatory immune response remains controversial. We aimed to study the impact of CRT on T cells in heart failure (HF) patients. Methods Thirty-nine HF patients were evaluated before CRT (T0) and six months later (T6). Quantification of T cells, their subsets, and their functional characterization, after in vitro stimulation, were evaluated by flow cytometry. Results T regulatory (Treg) cells were decreased in CHF patients (healthy group (HG): 1.08 ± 0.50 versus (heart failure patients (HFP)-T0: 0.69 ± 0.40, P = 0.022) and remaining diminished after CRT (HFP-T6: 0.61 ± 0.29, P = 0.003). Responders (R) to CRT presented a higher frequency of T cytotoxic (Tc) cells producing IL-2 at T0 compared with non-responders (NR) (R: 36.52 ± 12.55 versus NR: 24.71 ± 11.66, P = 0.006). After CRT, HF patients presented a higher percentage of Tc cells expressing TNF-α and IFN-γ (HG: 44.50 ± 16.62 versus R: 61.47 ± 20.54, P = 0.014; and HG: 40.62 ± 15.36 versus R: 52.39 ± 18.66, P = 0.049, respectively). Conclusion The dynamic of different functional T cell subpopulations is significantly altered in CHF, which results in an exacerbated pro-inflammatory response. Even after CRT, it seems that the inflammatory condition underlying CHF continues to evolve with the progression of the disease. This could be due, at least in part, to the inability to restore Treg cells levels.Springer Nature2023-02-15info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttps://hdl.handle.net/10316/111225https://hdl.handle.net/10316/111225https://doi.org/10.1186/s12872-023-03109-xeng1471-2261Martins, SílviaAntónio, NatáliaCarvalheiro, TiagoLaranjeira, PaulaRodrigues, RicardoGonçalves, LinoTomaz, CândidaPaiva, Arturinfo:eu-repo/semantics/openAccessreponame:Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)instname:FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiainstacron:RCAAP2024-01-05T12:17:50Zoai:estudogeral.uc.pt:10316/111225Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireinfo@rcaap.ptopendoar:https://opendoar.ac.uk/repository/71602025-05-29T06:03:09.632233Repositórios Científicos de Acesso Aberto de Portugal (RCAAP) - FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiafalse
dc.title.none.fl_str_mv Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
title Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
spellingShingle Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
Martins, Sílvia
Chronic heart failure
Cardiac resynchronization Therapy
Immune response
T cells
cytokines profile
Humans
T-Lymphocytes, Regulatory
Prospective Studies
Heart
Chronic Disease
Treatment Outcome
Cardiac Resynchronization Therapy
Heart Failure
title_short Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
title_full Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
title_fullStr Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
title_full_unstemmed Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
title_sort Reduced numbers of regulatory T cells in chronic heart failure seems not to be restored by cardiac resynchronization therapy
author Martins, Sílvia
author_facet Martins, Sílvia
António, Natália
Carvalheiro, Tiago
Laranjeira, Paula
Rodrigues, Ricardo
Gonçalves, Lino
Tomaz, Cândida
Paiva, Artur
author_role author
author2 António, Natália
Carvalheiro, Tiago
Laranjeira, Paula
Rodrigues, Ricardo
Gonçalves, Lino
Tomaz, Cândida
Paiva, Artur
author2_role author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Martins, Sílvia
António, Natália
Carvalheiro, Tiago
Laranjeira, Paula
Rodrigues, Ricardo
Gonçalves, Lino
Tomaz, Cândida
Paiva, Artur
dc.subject.por.fl_str_mv Chronic heart failure
Cardiac resynchronization Therapy
Immune response
T cells
cytokines profile
Humans
T-Lymphocytes, Regulatory
Prospective Studies
Heart
Chronic Disease
Treatment Outcome
Cardiac Resynchronization Therapy
Heart Failure
topic Chronic heart failure
Cardiac resynchronization Therapy
Immune response
T cells
cytokines profile
Humans
T-Lymphocytes, Regulatory
Prospective Studies
Heart
Chronic Disease
Treatment Outcome
Cardiac Resynchronization Therapy
Heart Failure
description Background T cells have been implicated in the development and progression of inflammatory processes in chronic heart failure (CHF). Cardiac resynchronization therapy (CRT) has beneficial effects on symptoms and cardiac remodeling in CHF. However, its impact on the inflammatory immune response remains controversial. We aimed to study the impact of CRT on T cells in heart failure (HF) patients. Methods Thirty-nine HF patients were evaluated before CRT (T0) and six months later (T6). Quantification of T cells, their subsets, and their functional characterization, after in vitro stimulation, were evaluated by flow cytometry. Results T regulatory (Treg) cells were decreased in CHF patients (healthy group (HG): 1.08 ± 0.50 versus (heart failure patients (HFP)-T0: 0.69 ± 0.40, P = 0.022) and remaining diminished after CRT (HFP-T6: 0.61 ± 0.29, P = 0.003). Responders (R) to CRT presented a higher frequency of T cytotoxic (Tc) cells producing IL-2 at T0 compared with non-responders (NR) (R: 36.52 ± 12.55 versus NR: 24.71 ± 11.66, P = 0.006). After CRT, HF patients presented a higher percentage of Tc cells expressing TNF-α and IFN-γ (HG: 44.50 ± 16.62 versus R: 61.47 ± 20.54, P = 0.014; and HG: 40.62 ± 15.36 versus R: 52.39 ± 18.66, P = 0.049, respectively). Conclusion The dynamic of different functional T cell subpopulations is significantly altered in CHF, which results in an exacerbated pro-inflammatory response. Even after CRT, it seems that the inflammatory condition underlying CHF continues to evolve with the progression of the disease. This could be due, at least in part, to the inability to restore Treg cells levels.
publishDate 2023
dc.date.none.fl_str_mv 2023-02-15
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 https://hdl.handle.net/10316/111225
https://hdl.handle.net/10316/111225
https://doi.org/10.1186/s12872-023-03109-x
url https://hdl.handle.net/10316/111225
https://doi.org/10.1186/s12872-023-03109-x
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 1471-2261
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Springer Nature
publisher.none.fl_str_mv Springer Nature
dc.source.none.fl_str_mv reponame:Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
instname:FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologia
instacron:RCAAP
instname_str FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologia
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reponame_str Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
collection Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
repository.name.fl_str_mv Repositórios Científicos de Acesso Aberto de Portugal (RCAAP) - FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologia
repository.mail.fl_str_mv info@rcaap.pt
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