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-1β 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-1β 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.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Kostadinova E,Chaput C,Gutbier B,Lippmann J,Sander LE,Mitchell TJ,Suttorp N,Witzenrath M,Opitz Bdoi
10.1038/srep30943subject
Has Abstractpub_date
2016-08-01 00:00:00pages
30943issn
2045-2322pii
srep30943journal_volume
6pub_type
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