NLRP3 protects alveolar barrier integrity by an inflammasome-independent increase of epithelial cell adherence
Research output: Contribution to journal › Article › peer-review
Colleges, School and Institutes
- Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.
- Institute of Microbiology and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15-2TT, UK.
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.
|Early online date||1 Aug 2016|
|Publication status||E-pub ahead of print - 1 Aug 2016|
- Journal Article, Bacterial infection, NOD-like receptors