Al-Awan, L

Audusseau, S

Chakir, J

Halayko, AJ

Hamid, Q

Lajoie-Kadoch, S

Lemière, C

Martin, JG

Mogas, AK

Olivenstein, R

Préfontaine, D

Allergy, Asthma & Clinical Immunology

English

PubMed

D Préfontaine

L Al-Awan

AK Mogas

S Audusseau

S Lajoie-Kadoch

R Olivenstein

J Chakir

AJ Halayko

C Lemière

JG Martin

Q Hamid

Springer - Publisher Connector

POSTER PRESENTATION 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, Q Hamid1*
From Canadian Society of Allergy and Clinical Immunology Annual Scientific Meeting 2009
Halifax, Canada. 22-25 October 2009
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 asth-
matic 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 con-
ditions seen in asthma promote IL-33 expression in
vitro. We also assessed whether IL-33 expression is sen-
sitive 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-a 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-
a-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-inflamma-
tory 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.
Author details
1Meakins-Christie Laboratories, Faculty of Medicine, McGill University, 3626
St-Urbain Street, Montreal, Qc, Canada H2X 2P2. 2Montreal Chest Hospital
Research Institute, McGill University, Canada. 3Faculty of Medecine, Laval
University, Quebec City, Canada. 4Faculty of Medecine, University of
Manitoba, Canada. 5Sacré-Coeur Hospital, University of Montreal, Canada.
Published: 12 May 2010
doi:10.1186/1710-1492-6-S1-P20
Cite this article as: Préfontaine et al.: Interleukin-33 in asthma: insights
into pro-inflammatory roles of airway structural cells. Allergy, Asthma &
Clinical Immunology 2010 6(Suppl 1):P20.
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* Correspondence: qutayba.hamid@mcgill.ca
1Meakins-Christie Laboratories, Faculty of Medicine, McGill University, 3626
St-Urbain Street, Montreal, Qc, Canada H2X 2P2
Préfontaine et al. Allergy, Asthma & Clinical Immunology 2010, 6(Suppl 1):P20
http://www.aacijournal.com/content/6/S1/P20 ALLERGY, ASTHMA & CLINICAL 
IMMUNOLOGY
© 2010 Préfontaine et al; licensee BioMed Central Ltd.


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

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

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