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...
| Autores: | , , , , , , , , |
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| 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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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 |
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article |
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publishedVersion |
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https://i3pt.portalinvestigacion.com/publicaciones/5155 |
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https://i3pt.portalinvestigacion.com/publicaciones/5155 |
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Inglés |
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Inglés |
| dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess |
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openAccess |
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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 instname:Institut d'Investigació i Innovació Parc Taulí (I3PT) |
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Institut d'Investigació i Innovació Parc Taulí (I3PT) |
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r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí |
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r-I3PT. Repositorio Institucional Producción Científica del Institut d'Investigació i Innovació Parc Taulí |
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