NLRP3 protects alveolar barrier integrity by an inflammasome-independent increase of epithelial cell adherence

Research output: Contribution to journalArticlepeer-review


  • Elena Kostadinova
  • Catherine Chaput
  • Birgitt Gutbier
  • Juliane Lippmann
  • Leif E Sander
  • Norbert Suttorp
  • Martin Witzenrath
  • Bastian Opitz

Colleges, School and Institutes

External organisations

  • 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.


Original languageEnglish
Article number30943
JournalScientific Reports
Early online date1 Aug 2016
Publication statusE-pub ahead of print - 1 Aug 2016


  • Journal Article, Bacterial infection, NOD-like receptors