Volume 6 Supplement 1

Canadian Society of Allergy and Clinical Immunology Annual Scientific Meeting 2009

Open Access

Interleukin-33 in asthma: insights into pro-inflammatory roles of airway structural cells

  • D Préfontaine1,
  • L Al-Awan1,
  • AK Mogas1,
  • S Audusseau1,
  • S Lajoie-Kadoch1,
  • R Olivenstein2,
  • J Chakir3,
  • AJ Halayko4,
  • C Lemière5,
  • JG Martin1 and
  • Q Hamid1Email author
Allergy, Asthma & Clinical Immunology20106(Suppl 1):P20


Published: 12 May 2010


Interleukin-33 (IL-33) is a novel cytokine that triggers inflammatory immune responses, but evidence of its role in human asthma, a common allergic airway disease, is lacking. There is also a paucity of information regarding which cells express IL-33, and what conditions promote its expression. We sought to investigate whether IL-33 is expressed in the lung tissue from patients with asthma.


We obtained lung biopsy tissue specimens from asthmatic adults and from healthy control subjects, along with normal primary cells from human airways that were cultured in vitro. We studied expression of IL-33 in lung tissue specimens, and determined whether conditions seen in asthma promote IL-33 expression in vitro. We also assessed whether IL-33 expression is sensitive to glucocorticoid treatment.


Higher expression of IL-33 is detected in lung tissue from asthmatic patients compared to control subjects. IL-33 expression correlates TNF-α e.g. a hallmark of inflammation. Airway epithelium, smooth muscle cells and endothelium are all sources of IL-33. When exposed to inflammatory conditions, in vitro cultured bronchial smooth muscle and epithelial cells increased their IL-33 expression, which surprisingly remained intracellular. Finally, glucocorticoid did not significantly reduce TNF-α-induced IL-33 expression.


Our study first describes IL-33 expression in asthma; it is increased in the lungs from asthmatics, and is enhanced under asthma-like in vitro conditions. IL-33 originates from structural cells of the airways and its expression does not respond to classic anti-inflammatory drug, thus reinforcing its relevance as a potential therapeutic target to treat asthma.

Research funding sources

Severe Asthma Program – Richard & Edith Strauss Canada Foundation. J.T. Costello Memorial Research Fund. Fonds de Recherche en Santé du Québec.

Authors’ Affiliations

Meakins-Christie Laboratories, Faculty of Medicine, McGill University
Montreal Chest Hospital Research Institute, McGill University
Faculty of Medecine, Laval University
Faculty of Medecine, University of Manitoba
Sacré-Coeur Hospital, University of Montreal


© Préfontaine and Hamid; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd.