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IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice

Title
IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice
Authors
Cho K.-A.Suh J.W.Sohn J.H.Park J.W.Lee H.Kang J.L.Woo S.-Y.Cho Y.J.
Ewha Authors
이지희조영주우소연조경아
SCOPUS Author ID
이지희scopus; 조영주scopus; 우소연scopus; 조경아scopus
Issue Date
2012
Journal Title
American Journal of Physiology - Lung Cellular and Molecular Physiology
ISSN
1040-0605JCR Link
Citation
vol. 302, no. 4, pp. L429 - L440
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Allergic asthma is characterized by infiltration of eosinophils, elevated Th2 cytokine levels, airway hyperresponsiveness, and IgE. In addition to eosinophils, mast cells, and basophils, a variety of cytokines are also involved in the development of allergic asthma. The pivotal role of eosinophils in the progression of the disease has been a subject of controversy. To determine the role of eosinophils in the progression of airway inflammation, we sensitized and challenged BALB/c wild-type (WT) mice and eosinophil-deficient ΔdblGATA mice with ovalbumin (OVA) and analyzed different aspects of inflammation. We observed increased eosinophil levels and a Th2-dominant response in OVA-challenged WT mice. In contrast, eosinophil-deficient ΔdblGATA mice displayed an increased proportion of mast cells and a Th17-biased response following OVA inhalation. Notably, the levels of IL-33, an important cytokine responsible for Th2 immune deviation, were not different between WT and eosinophil-deficient mice. We also demonstrated that mast cells induced Th17-differentiation via IL-33/ST2 stimulation in vitro. These results indicate that eosinophils are not essential for the development of allergic asthma and that mast cells can skew the immune reaction predominantly toward Th17 responses via IL-33 stimulation. © 2012 the American Physiological Society.
DOI
10.1152/ajplung.00252.2011
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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