Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury

Background: In the early stages of acute respiratory distress syndrome (ARDS), pro-inflammatory mediators inhibit natural anticoagulant factors and initiate an increase in procoagulant activity. Previous studies proved the beneficial effects of heparin in pulmonary coagulopathy, which derive from it...

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Autores: Camprubí-Rimblas, M, Guillamat-Prats, R, Lebouvier, T, Bringué, J, Chimenti, L, Iglesias, M, Obiols, C, Tijero, J, Blanch, L, Artigas, A
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:España
Institución:Institut d'Investigació i Innovació Parc Taulí (I3PT)
Repositorio:r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí
OAI Identifier:oai:i3pt.fundanetsuite.com:p4606
Acceso en línea:https://i3pt.portalinvestigacion.com/publicaciones/4606
Access Level:acceso abierto
Palabra clave:Acute Respiratory Distress Syndrome (ARDS)
Alveolar macrophages
Alveolar cells
Fibroblasts
Anticoagulants
Inflammation
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spelling Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injuryCamprubí-Rimblas, MGuillamat-Prats, RLebouvier, TBringué, JChimenti, LIglesias, MObiols, CTijero, JBlanch, LArtigas, AAcute Respiratory Distress Syndrome (ARDS)Alveolar macrophagesAlveolar cellsFibroblastsAnticoagulantsInflammationBackground: In the early stages of acute respiratory distress syndrome (ARDS), pro-inflammatory mediators inhibit natural anticoagulant factors and initiate an increase in procoagulant activity. Previous studies proved the beneficial effects of heparin in pulmonary coagulopathy, which derive from its anticoagulant and anti-inflammatory activities, although it is uncertain whether heparin works. Understanding the specific effect of unfractioned heparin on cell lung populations would be of interest to increase our knowledge about heparin pathways and to treat ARDS. Methods: In the current study, the effect of heparin was assessed in primary human alveolar macrophages ( hAM), alveolar type II cells (hATII), and fibroblasts (hF) that had been injured with LPS. Results: Heparin did not produce any changes in the Smad/TGF beta pathway, in any of the cell types evaluated. Heparin reduced the expression of pro-inflammatory markers (TNF-alpha and IL-6) in hAM and deactivated the NF-k beta pathway in hATII, diminishing the expression of IRAK1 and MyD88 and their effectors, IL-6, MCP-1 and IL-8. Conclusions: The current study demonstrated that heparin significantly ameliorated the cells lung injury induced by LPS through the inhibition of pro-inflammatory cytokine expression in macrophages and the NF-k beta pathway in alveolar cells. Our results suggested that a local pulmonary administration of heparin through nebulization may be able to reduce inflammation in the lung; however, further studies are needed to confirm this hypothesis.BMC2017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://i3pt.portalinvestigacion.com/publicaciones/4606RESPIRATORY RESEARCHISSN: 1465993Xreponame:r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulíinstname:Institut d'Investigació i Innovació Parc Taulí (I3PT)Inglésinfo:eu-repo/semantics/openAccessoai:i3pt.fundanetsuite.com:p46062026-06-21T15:30:37Z
dc.title.none.fl_str_mv Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
title Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
spellingShingle Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
Camprubí-Rimblas, M
Acute Respiratory Distress Syndrome (ARDS)
Alveolar macrophages
Alveolar cells
Fibroblasts
Anticoagulants
Inflammation
title_short Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
title_full Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
title_fullStr Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
title_full_unstemmed Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
title_sort Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury
dc.creator.none.fl_str_mv Camprubí-Rimblas, M
Guillamat-Prats, R
Lebouvier, T
Bringué, J
Chimenti, L
Iglesias, M
Obiols, C
Tijero, J
Blanch, L
Artigas, A
author Camprubí-Rimblas, M
author_facet Camprubí-Rimblas, M
Guillamat-Prats, R
Lebouvier, T
Bringué, J
Chimenti, L
Iglesias, M
Obiols, C
Tijero, J
Blanch, L
Artigas, A
author_role author
author2 Guillamat-Prats, R
Lebouvier, T
Bringué, J
Chimenti, L
Iglesias, M
Obiols, C
Tijero, J
Blanch, L
Artigas, A
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Acute Respiratory Distress Syndrome (ARDS)
Alveolar macrophages
Alveolar cells
Fibroblasts
Anticoagulants
Inflammation
topic Acute Respiratory Distress Syndrome (ARDS)
Alveolar macrophages
Alveolar cells
Fibroblasts
Anticoagulants
Inflammation
description Background: In the early stages of acute respiratory distress syndrome (ARDS), pro-inflammatory mediators inhibit natural anticoagulant factors and initiate an increase in procoagulant activity. Previous studies proved the beneficial effects of heparin in pulmonary coagulopathy, which derive from its anticoagulant and anti-inflammatory activities, although it is uncertain whether heparin works. Understanding the specific effect of unfractioned heparin on cell lung populations would be of interest to increase our knowledge about heparin pathways and to treat ARDS. Methods: In the current study, the effect of heparin was assessed in primary human alveolar macrophages ( hAM), alveolar type II cells (hATII), and fibroblasts (hF) that had been injured with LPS. Results: Heparin did not produce any changes in the Smad/TGF beta pathway, in any of the cell types evaluated. Heparin reduced the expression of pro-inflammatory markers (TNF-alpha and IL-6) in hAM and deactivated the NF-k beta pathway in hATII, diminishing the expression of IRAK1 and MyD88 and their effectors, IL-6, MCP-1 and IL-8. Conclusions: The current study demonstrated that heparin significantly ameliorated the cells lung injury induced by LPS through the inhibition of pro-inflammatory cytokine expression in macrophages and the NF-k beta pathway in alveolar cells. Our results suggested that a local pulmonary administration of heparin through nebulization may be able to reduce inflammation in the lung; however, further studies are needed to confirm this hypothesis.
publishDate 2017
dc.date.none.fl_str_mv 2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://i3pt.portalinvestigacion.com/publicaciones/4606
url https://i3pt.portalinvestigacion.com/publicaciones/4606
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv BMC
publisher.none.fl_str_mv BMC
dc.source.none.fl_str_mv RESPIRATORY RESEARCH
ISSN: 1465993X
reponame:r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí
instname:Institut d'Investigació i Innovació Parc Taulí (I3PT)
instname_str Institut d'Investigació i Innovació Parc Taulí (I3PT)
reponame_str r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí
collection r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí
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