Analysis of pollen-driven endogenous IL-33 and basophils in allergic rhinitis manifestation

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390253
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: 膠原病・アレルギー・感染症内科学
• Research Institution: Hyogo Medical University
• Principal Investigator: YOSHIMOTO Tomohiro 兵庫医科大学, 医学部, 教授 (60241171)
• Co-Investigator(Kenkyū-buntansha): MATSUSHITA Kazufumi 兵庫医科大学, 医学部, 講師 (20581549) ; YASUDA Koubun 兵庫医科大学, 医学部, 講師 (50333539) ; MATSUMOTO Makoto 兵庫医科大学, 医学部, 講師 (40380521)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: アレルギー性鼻炎 / IL-33 / 好塩基球 / 好酸球 / 花粉 / モデルマウス

Outline of Final Research Achievements

We established a novel mouse model of ragweed (RW) pollen-specific allergic rhinitis (AR) and examined the pathological role for endogenous IL-33 in the induction of early- and late-phase AR manifestation using IL-33-deficient mice. After nasal challenge with RW pollen, RW-immunized wild-type mice manifested early-phase (sneezing), and late-phase (eosinophilic/basophilic accumulation) responses. In contrast, IL-33-deficient and basophils-depleted mice failed to develop AR. We revealed that IL-33-stimulated mast cells and basophils contribute to sneezing and accumulation of eosinophils/basophils in the nasal mucosa by increasing histamine release and production of chemoattractants for eosinophils/basophils, respectively. Finally, compared with healthy controls, IL-33 mRNA expression in nasal epithelial cells from AR patients significantly increased during the pollen season. Thus, RW pollen-driven endogenous IL-33 and basophils are promising therapeutic target molecules to prevent AR.

Free Research Field

免疫学