Table of Contents
Journal of Allergy
Volume 2012 (2012), Article ID 819176, 13 pages
Research Article

Immunolocalization of NLRP3 Inflammasome in Normal Murine Airway Epithelium and Changes following Induction of Ovalbumin-Induced Airway Inflammation

1Centre for Inflammatory Disease Research (CIDR), The Basil Hetzel Institute for Translational Health Research, Woodville South, SA 5011, Australia
2Stroke Research Programme and Neurology Department, University of Adelaide School of Medicine, The Queen Elizabeth Hospital, Woodville South, SA 5011, Australia
3School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, SA 5005, Australia
4Department of Surgery–Otorhinolaryngology Head and Neck Surgery, University of Adelaide, The Queen Elizabeth Hospital, Woodville South, SA 5011, Australia
5Rheumatology Department, The Queen Elizabeth Hospital, Woodville Road, Woodville South, SA 5011, Australia
6Discipline of Medicine 5B, University of Adelaide, The Queen Elizabeth Hospital, Woodville South, SA 5011, Australia

Received 14 June 2011; Revised 15 August 2011; Accepted 4 December 2011

Academic Editor: Darryl A. Knight

Copyright © 2012 Hai B. Tran et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Little is known about innate immunity and components of inflammasomes in airway epithelium. This study evaluated immunohistological evidence for NLRP3 inflammasomes in normal and inflamed murine (Balb/c) airway epithelium in a model of ovalbumin (OVA) induced allergic airway inflammation. The airway epithelium of control mice exhibited strong cytoplasmic staining for total caspase-1, ASC, and NLRP3, whereas the OVA mice exhibited strong staining for active caspase-1, with redistribution of caspase-1, IL-1β and IL-18, indicating possible activation of the NLRP3 inflammasome. Active caspase-1, NLRP3, and other inflammasome components were also detected in tissue eosinophils from OVA mice, and may potentially contribute to IL-1β and IL-18 production. In whole lung, inRNA expression of NAIP and procaspase-1 was increased in OVA mice, whereas NLRP3, IL-1β and IL-18 decreased. Some OVA-treated mice also had significantly elevated and tightly correlated serum levels of IL-1β and TNFα. In cultured normal human bronchial epithelial cells, LPS priming resulted in a significant increase in NLRP3 and II-lp protein expression. This study is the first to demonstrate NLRP3 inflammasome components in normal airway epithelium and changes with inflammation. We propose activation and/or luminal release of the inflammasome is a feature of allergic airway inflammation which may contribute to disease pathogenesis.