Edited by: Angela Haczku
NLRP3 inflammasome is required in murine asthma in the absence of aluminum adjuvant
Article first published online: 28 MAR 2011
© 2011 John Wiley & Sons A/S
Volume 66, Issue 8, pages 1047–1057, August 2011
How to Cite
Besnard, A.-G., Guillou, N., Tschopp, J., Erard, F., Couillin, I., Iwakura, Y., Quesniaux, V., Ryffel, B. and Togbe, D. (2011), NLRP3 inflammasome is required in murine asthma in the absence of aluminum adjuvant. Allergy, 66: 1047–1057. doi: 10.1111/j.1398-9995.2011.02586.x
- Issue published online: 5 JUL 2011
- Article first published online: 28 MAR 2011
- Accepted for publication 2 March 2011
- allergic inflammation;
- NLRP3 inflammasome
To cite this article: Besnard A-G, Guillou N, Tschopp J, Erard F, Couillin I, Iwakura Y, Quesniaux V, Ryffel B, Togbe D. NLRP3 inflammasome is required in murine asthma in the absence of aluminum adjuvant. Allergy 2011; 66: 1047–1057.
Background: Inflammasome activation with the production of IL-1β received substantial attention recently in inflammatory diseases. However, the role of inflammasome in the pathogenesis of asthma is not clear. Using an adjuvant-free model of allergic lung inflammation induced by ovalbumin (OVA), we investigated the role of NLRP3 inflammasome and related it to IL-1R1 signaling pathway.
Methods: Allergic lung inflammation induced by OVA was evaluated in vivo in mice deficient in NLRP3 inflammasome, IL-1R1, IL-1β or IL-1α. Eosinophil recruitment, Th2 cytokine, and chemokine levels were determined in bronchoalveolar lavage fluid, lung homogenates, and mediastinal lymph node cells ex vivo.
Results: Allergic airway inflammation depends on NLRP3 inflammasome activation. Dendritic cell recruitment into lymph nodes, Th2 lymphocyte activation in the lung and secretion of Th2 cytokines and chemokines are reduced in the absence of NLRP3. Absence of NLRP3 and IL-1β is associated with reduced expression of other proinflammatory cytokines such as IL-5, IL-13, IL-33, and thymic stromal lymphopoietin. Furthermore, the critical role of IL-1R1 signaling in allergic inflammation is confirmed in IL-1R1-, IL-1β-, and IL-1α-deficient mice.
Conclusion: NLRP3 inflammasome activation leading to IL-1 production is critical for the induction of a Th2 inflammatory allergic response.