NLRP3 protects alveolar barrier integrity by an inflammasome-independent increase of epithelial cell adherence.
Sci Rep
; 6: 30943, 2016 08 01.
Article
en En
| MEDLINE
| ID: mdl-27476670
ABSTRACT
Bacterial pneumonia is a major cause of acute lung injury and acute respiratory distress syndrome, characterized by alveolar barrier disruption. NLRP3 is best known for its ability to form inflammasomes and to regulate IL-1ß and IL-18 production in myeloid cells. Here we show that NLRP3 protects the integrity of the alveolar barrier in a mouse model of Streptococcus pneumoniae-induced pneumonia, and ex vivo upon treatment of isolated perfused and ventilated lungs with the purified bacterial toxin, pneumolysin. We reveal that the preserving effect of NLRP3 on the lung barrier is independent of inflammasomes, IL-1ß and IL-18. NLRP3 improves the integrity of alveolar epithelial cell monolayers by enhancing cellular adherence. Collectively, our study uncovers a novel function of NLRP3 by demonstrating that it protects epithelial barrier function independently of inflammasomes.
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Neumonía Neumocócica
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Alveolos Pulmonares
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Células Epiteliales
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Lesión Pulmonar Inducida por Ventilación Mecánica
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Inflamasomas
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Proteína con Dominio Pirina 3 de la Familia NLR
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Sci Rep
Año:
2016
Tipo del documento:
Article
País de afiliación:
Alemania