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

Kyung Ah Cho, Jee Won Suh, Jung Ho Sohn, Jung Won Park, Hyejin Lee, Ji Hee Lee Kang, So Youn Woo, Young Joo Cho

Research output: Contribution to journalArticle

42 Citations (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.

Original languageEnglish
Pages (from-to)L429-L440
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume302
Issue number4
DOIs
Publication statusPublished - 2012 Feb 1

Fingerprint

Ovalbumin
Eosinophils
Mast Cells
Inflammation
Asthma
Cytokines
Interleukin-33
Basophils
Immunoglobulin E
Inhalation
Disease Progression

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

Cite this

Cho, Kyung Ah ; Suh, Jee Won ; Sohn, Jung Ho ; Park, Jung Won ; Lee, Hyejin ; Kang, Ji Hee Lee ; Woo, So Youn ; Cho, Young Joo. / IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2012 ; Vol. 302, No. 4. pp. L429-L440.
@article{65d1fac2412843018302bc90cd8f336a,
title = "IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice",
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.",
author = "Cho, {Kyung Ah} and Suh, {Jee Won} and Sohn, {Jung Ho} and Park, {Jung Won} and Hyejin Lee and Kang, {Ji Hee Lee} and Woo, {So Youn} and Cho, {Young Joo}",
year = "2012",
month = "2",
day = "1",
doi = "10.1152/ajplung.00252.2011",
language = "English",
volume = "302",
pages = "L429--L440",
journal = "American Journal of Physiology - Lung Cellular and Molecular Physiology",
issn = "1040-0605",
publisher = "American Physiological Society",
number = "4",

}

IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice. / Cho, Kyung Ah; Suh, Jee Won; Sohn, Jung Ho; Park, Jung Won; Lee, Hyejin; Kang, Ji Hee Lee; Woo, So Youn; Cho, Young Joo.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 302, No. 4, 01.02.2012, p. L429-L440.

Research output: Contribution to journalArticle

TY - JOUR

T1 - IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice

AU - Cho, Kyung Ah

AU - Suh, Jee Won

AU - Sohn, Jung Ho

AU - Park, Jung Won

AU - Lee, Hyejin

AU - Kang, Ji Hee Lee

AU - Woo, So Youn

AU - Cho, Young Joo

PY - 2012/2/1

Y1 - 2012/2/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84863022201&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84863022201&partnerID=8YFLogxK

U2 - 10.1152/ajplung.00252.2011

DO - 10.1152/ajplung.00252.2011

M3 - Article

C2 - 22180658

AN - SCOPUS:84863022201

VL - 302

SP - L429-L440

JO - American Journal of Physiology - Lung Cellular and Molecular Physiology

JF - American Journal of Physiology - Lung Cellular and Molecular Physiology

SN - 1040-0605

IS - 4

ER -