Distinct effects of endogenous interleukin-23 on eosinophilic airway inflammation in response to different antigens

Rika Ogawa, Yusuke Suzuki, Shizuko Kagawa, Katsunori Masaki, Koichi Fukunaga, Akihiko Yoshimura, Seitaro Fujishima, Takeshi Terashima, Tomoko Betsuyaku, Koichiro Asano

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6 Citations (Scopus)


Background The role of interleukin (IL)-23 in asthma pathophysiology is still controversial. We examined its role in allergic airway inflammation in response to two distinct antigens using IL-23-deficient mice. Methods Allergic airway inflammation was evaluated in wild-type and IL-23p19-/- mice. Mice were sensitized to ovalbumin (OVA) or house dust mite (HDM) by intraperitoneal injection of antigen and their airways were then exposed to the same antigen. Levels of antigen-specific immunoglobulins in serum as well as cytokines in bronchoalveolar or peritoneal lavage fluid and lung tissue were determined by enzyme-linked immunosorbent assay and/or quantitative polymerase chain reaction. Results Deficiency of IL-23p19 decreased eosinophils and Th2 cytokines in bronchoalveolar lavage fluid (BALF) of OVA-treated mice, while it increased BALF eosinophils of HDM-treated mice. Peritoneal injection of OVA with alum, but not of HDM, induced local synthesis of IL-6, IL-10, and IL-23. Systemic production of antigen-specific IgG1 was partially dependent on IL-23. In contrast, airway exposure to HDM, but not to OVA, induced IL-23p19 mRNA expression in the lungs. In IL-23p19-deficient mice, HDM-exposed lungs did not exhibit the induction of IL-17A, which negatively regulates eosinophilic inflammation. Conclusions Different antigens induced IL-23 at different part of the body in our similar asthma models. Endogenous IL-23 production at the site of antigen sensitization facilitates type-2 immune responses, whereas IL-23 production and subsequent IL-17A synthesis in the airways suppresses allergic inflammation.

Original languageEnglish
Article number67
Pages (from-to)S24-S29
JournalAllergology International
Publication statusPublished - 2015 Sept 1


  • Asthma
  • Eosinophils
  • Interleukin-17A
  • Interleukin-23
  • Th17

ASJC Scopus subject areas

  • Immunology and Allergy


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