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Logo of aaciBioMed CentralBiomed Central Web Sitesearchsubmit a manuscriptregisterthis articleAllergy, Asthma, and Clinical Immunology : Official Journal of the Canadian Society of Allergy and Clinical Immunology
 
Allergy Asthma Clin Immunol. 2010; 6(Suppl 1): P20.
Published online 2010 May 12. doi:  10.1186/1710-1492-6-S1-P20
PMCID: PMC2874290

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

Abstract

Background

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.

Methods

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.

Results

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.

Conclusions

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.


Articles from Allergy, Asthma, and Clinical Immunology : Official Journal of the Canadian Society of Allergy and Clinical Immunology are provided here courtesy of BioMed Central