Acute exposure to silica nanoparticles enhances mortality and increases lung permeability in a mouse model of Pseudomonas aeruginosa pneumonia.
hal.structure.identifier | Unité de Biologie Fonctionnelle et Adaptative [BFA (UMR_8251 / U1133)] | |
dc.contributor.author | DELAVAL, Mathilde | |
hal.structure.identifier | Unité de Biologie Fonctionnelle et Adaptative [BFA (UMR_8251 / U1133)] | |
dc.contributor.author | BOLAND, Sonja | |
hal.structure.identifier | Défense innée et inflammation | |
hal.structure.identifier | Physiopathologie et Epidémiologie des Maladies Respiratoires [PHERE (UMR_S_1152 / U1152)] | |
dc.contributor.author | SOLHONNE, Brigitte | |
hal.structure.identifier | Imagerie Dynamique (Plate-Forme) [PFID] | |
dc.contributor.author | NICOLA, Marie-Anne | |
hal.structure.identifier | Institut de Chimie de la Matière Condensée de Bordeaux [ICMCB] | |
dc.contributor.author | MORNET, Stéphane | |
hal.structure.identifier | Unité de Biologie Fonctionnelle et Adaptative [BFA (UMR_8251 / U1133)] | |
dc.contributor.author | BAEZA-SQUIBAN, Armelle | |
hal.structure.identifier | Cellule Pasteur | |
hal.structure.identifier | Défense innée et inflammation | |
hal.structure.identifier | Physiopathologie et Epidémiologie des Maladies Respiratoires [PHERE (UMR_S_1152 / U1152)] | |
dc.contributor.author | SALLENAVE, Jean-Michel | |
hal.structure.identifier | Défense innée et inflammation | |
hal.structure.identifier | Physiopathologie et Epidémiologie des Maladies Respiratoires [PHERE (UMR_S_1152 / U1152)] | |
hal.structure.identifier | Cellule Pasteur | |
dc.contributor.author | GARCIA-VERDUGO, Ignacio | |
dc.date.issued | 2014-11-30 | |
dc.identifier.issn | 1743-8977 | |
dc.description.abstractEn | The lung epithelium constitutes the first barrier against invading pathogens and also a major surface potentially exposed to nanoparticles. In order to ensure and preserve lung epithelial barrier function, the alveolar compartment possesses local defence mechanisms that are able to control bacterial infection. For instance, alveolar macrophages are professional phagocytic cells that engulf bacteria and environmental contaminants (including nanoparticles) and secrete pro-inflammatory cytokines to effectively eliminate the invading bacteria/contaminants. The consequences of nanoparticle exposure in the context of lung infection have not been studied in detail. Previous reports have shown that sequential lung exposure to nanoparticles and bacteria may impair bacterial clearance resulting in increased lung bacterial loads, associated with a reduction in the phagocytic capacity of alveolar macrophages. Here we have studied the consequences of SiO2 nanoparticle exposure on Pseudomonas aeruginosa clearance, Pseudomonas aeruginosa-induced inflammation and lung injury in a mouse model of acute pneumonia. We observed that pre-exposure to SiO2 nanoparticles increased mice susceptibility to lethal pneumonia but did not modify lung clearance of a bioluminescent Pseudomonas aeruginosa strain. Furthermore, internalisation of SiO2 nanoparticles by primary alveolar macrophages did not reduce the capacity of the cells to clear Pseudomonas aeruginosa. In our murine model, SiO2 nanoparticle pre-exposure preferentially enhanced Pseudomonas aeruginosa-induced lung permeability (the latter assessed by the measurement of alveolar albumin and IgM concentrations) rather than contributing to Pseudomonas aeruginosa-induced lung inflammation (as measured by leukocyte recruitment and cytokine concentration in the alveolar compartment). We show that pre-exposure to SiO2 nanoparticles increases mice susceptibility to lethal pneumonia but independently of macrophage phagocytic function. The deleterious effects of SiO2 nanoparticle exposure during Pseudomonas aeruginosa-induced pneumonia are related to alterations of the alveolar-capillary barrier rather than to modulation of the inflammatory responses. | |
dc.language.iso | en | |
dc.publisher | BioMed Central | |
dc.subject.en | Alveolar permeability | |
dc.subject.en | Inflammation | |
dc.subject.en | Infection | |
dc.subject.en | Alveolar macrophages | |
dc.subject.en | SiO2 | |
dc.subject.en | Nanoparticles | |
dc.subject.en | Pseudomonas | |
dc.subject.en | Lung | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Bronchoalveolar Lavage Fluid | |
dc.subject.mesh | Surface Properties | |
dc.subject.mesh | Survival Analysis | |
dc.subject.mesh | Capillary Permeability | |
dc.subject.mesh | Cytokines | |
dc.subject.mesh | Immunoglobulin M | |
dc.subject.mesh | Inhalation Exposure | |
dc.subject.mesh | Macrophages, Alveolar | |
dc.subject.mesh | Male | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Nanoparticles | |
dc.subject.mesh | Particle Size | |
dc.subject.mesh | Phagocytosis | |
dc.subject.mesh | Pneumonia, Bacterial | |
dc.subject.mesh | Pseudomonas Infections | |
dc.subject.mesh | Pseudomonas aeruginosa | |
dc.subject.mesh | Pulmonary Alveoli | |
dc.subject.mesh | Selenium Oxides | |
dc.title.en | Acute exposure to silica nanoparticles enhances mortality and increases lung permeability in a mouse model of Pseudomonas aeruginosa pneumonia. | |
dc.type | Article de revue | |
dc.identifier.doi | 10.1186/s12989-014-0078-9 | |
dc.subject.hal | Sciences du Vivant [q-bio] | |
bordeaux.journal | Particle and Fibre Toxicology | |
bordeaux.page | 1 | |
bordeaux.volume | 12 | |
bordeaux.issue | 1 | |
bordeaux.peerReviewed | oui | |
hal.identifier | inserm-01264515 | |
hal.version | 1 | |
hal.popular | non | |
hal.audience | Internationale | |
hal.origin.link | https://hal.archives-ouvertes.fr//inserm-01264515v1 | |
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