Endotoxin-induced lung alveolar cell injury causes brain cell damage

Sepsis is the most common cause of acute respiratory distress syndrome, a severe lung inflammatory disorder with an elevated morbidity and mortality. Sepsis and acute respiratory distress syndrome involve the release of inflammatory mediators to the systemic circulation, propagating the cellular and...

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Autores: Rodríguez-González, R, Ramos-Nuez, A, Martín-Barrasa, JL, López-Aguilar, J, Baluja, A, Alvarez, J, Rocco, PRM, Pelosi, P, Villar, J
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2015
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:p5155
Acceso en línea:https://i3pt.portalinvestigacion.com/publicaciones/5155
Access Level:acceso abierto
Palabra clave:Sepsis
lung injury
apoptosis
acute respiratory distress syndrome
brain injury
inflammation
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spelling Endotoxin-induced lung alveolar cell injury causes brain cell damageRodríguez-González, RRamos-Nuez, AMartín-Barrasa, JLLópez-Aguilar, JBaluja, AAlvarez, JRocco, PRMPelosi, PVillar, JSepsislung injuryapoptosisacute respiratory distress syndromebrain injuryinflammationSepsis is the most common cause of acute respiratory distress syndrome, a severe lung inflammatory disorder with an elevated morbidity and mortality. Sepsis and acute respiratory distress syndrome involve the release of inflammatory mediators to the systemic circulation, propagating the cellular and molecular response and affecting distal organs, including the brain. Since it has been reported that sepsis and acute respiratory distress syndrome contribute to brain dysfunction, we investigated the brain-lung crosstalk using a combined experimental invitro airway epithelial and brain cell injury model. Conditioned medium collected from an invitro lipopolysaccharide-induced airway epithelial cell injury model using human A549 alveolar cells was subsequently added at increasing concentrations (no conditioned, 2%, 5%, 10%, 15%, 25%, and 50%) to a rat mixed brain cell culture containing both astrocytes and neurons. Samples from culture media and cells from mixed brain cultures were collected before treatment, and at 6 and 24h for analysis. Conditioned medium at 15% significantly increased apoptosis in brain cell cultures 24h after treatment, whereas 25% and 50% significantly increased both necrosis and apoptosis. Levels of brain damage markers S100 calcium binding protein B and neuron-specific enolase, interleukin-6, macrophage inflammatory protein-2, as well as matrix metalloproteinase-9 increased significantly after treating brain cells with 2% conditioned medium. Our findings demonstrated that human epithelial pulmonary cells stimulated with bacterial lipopolysaccharide release inflammatory mediators that are able to induce a translational clinically relevant and harmful response in brain cells. These results support a brain-lung crosstalk during sepsis and sepsis-induced acute respiratory distress syndrome.FRONTIERS MEDIA SA2015info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://i3pt.portalinvestigacion.com/publicaciones/5155EXPERIMENTAL BIOLOGY AND MEDICINEISSN: 15353702ISSNe: 15353699reponame: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:p51552026-06-21T15:30:37Z
dc.title.none.fl_str_mv Endotoxin-induced lung alveolar cell injury causes brain cell damage
title Endotoxin-induced lung alveolar cell injury causes brain cell damage
spellingShingle Endotoxin-induced lung alveolar cell injury causes brain cell damage
Rodríguez-González, R
Sepsis
lung injury
apoptosis
acute respiratory distress syndrome
brain injury
inflammation
title_short Endotoxin-induced lung alveolar cell injury causes brain cell damage
title_full Endotoxin-induced lung alveolar cell injury causes brain cell damage
title_fullStr Endotoxin-induced lung alveolar cell injury causes brain cell damage
title_full_unstemmed Endotoxin-induced lung alveolar cell injury causes brain cell damage
title_sort Endotoxin-induced lung alveolar cell injury causes brain cell damage
dc.creator.none.fl_str_mv Rodríguez-González, R
Ramos-Nuez, A
Martín-Barrasa, JL
López-Aguilar, J
Baluja, A
Alvarez, J
Rocco, PRM
Pelosi, P
Villar, J
author Rodríguez-González, R
author_facet Rodríguez-González, R
Ramos-Nuez, A
Martín-Barrasa, JL
López-Aguilar, J
Baluja, A
Alvarez, J
Rocco, PRM
Pelosi, P
Villar, J
author_role author
author2 Ramos-Nuez, A
Martín-Barrasa, JL
López-Aguilar, J
Baluja, A
Alvarez, J
Rocco, PRM
Pelosi, P
Villar, J
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Sepsis
lung injury
apoptosis
acute respiratory distress syndrome
brain injury
inflammation
topic Sepsis
lung injury
apoptosis
acute respiratory distress syndrome
brain injury
inflammation
description Sepsis is the most common cause of acute respiratory distress syndrome, a severe lung inflammatory disorder with an elevated morbidity and mortality. Sepsis and acute respiratory distress syndrome involve the release of inflammatory mediators to the systemic circulation, propagating the cellular and molecular response and affecting distal organs, including the brain. Since it has been reported that sepsis and acute respiratory distress syndrome contribute to brain dysfunction, we investigated the brain-lung crosstalk using a combined experimental invitro airway epithelial and brain cell injury model. Conditioned medium collected from an invitro lipopolysaccharide-induced airway epithelial cell injury model using human A549 alveolar cells was subsequently added at increasing concentrations (no conditioned, 2%, 5%, 10%, 15%, 25%, and 50%) to a rat mixed brain cell culture containing both astrocytes and neurons. Samples from culture media and cells from mixed brain cultures were collected before treatment, and at 6 and 24h for analysis. Conditioned medium at 15% significantly increased apoptosis in brain cell cultures 24h after treatment, whereas 25% and 50% significantly increased both necrosis and apoptosis. Levels of brain damage markers S100 calcium binding protein B and neuron-specific enolase, interleukin-6, macrophage inflammatory protein-2, as well as matrix metalloproteinase-9 increased significantly after treating brain cells with 2% conditioned medium. Our findings demonstrated that human epithelial pulmonary cells stimulated with bacterial lipopolysaccharide release inflammatory mediators that are able to induce a translational clinically relevant and harmful response in brain cells. These results support a brain-lung crosstalk during sepsis and sepsis-induced acute respiratory distress syndrome.
publishDate 2015
dc.date.none.fl_str_mv 2015
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/5155
url https://i3pt.portalinvestigacion.com/publicaciones/5155
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 FRONTIERS MEDIA SA
publisher.none.fl_str_mv FRONTIERS MEDIA SA
dc.source.none.fl_str_mv EXPERIMENTAL BIOLOGY AND MEDICINE
ISSN: 15353702
ISSNe: 15353699
reponame:r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí
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instname_str Institut d'Investigació i Innovació Parc Taulí (I3PT)
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