Thursday, 15 October 2015: 16:00 - 16:15
Room R2 ABC (Floor 3) (Coex Convention Center)
Da-Eun Park
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Hyun Seung Lee
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Woo-Jung Song, MD
,
Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea
Hye-Ryun Kang, MD, PhD
,
Regional Pharmacovigilance Center, Seoul National University Hospital, Seoul, South Korea
Heung Woo Park, MD, PhD
,
Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea
Yoon-Seok Chang, MD, PhD
,
Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea
Jung-Won Park, MD, PhD
,
Division of Allergy and Immunology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea
Sang-Heon Cho, MD, PhD
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Kyung-up Min, MD, PhD
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Background: IL-23 has been postulated to be a critical mediator contributing to airway inflammation. House dust mite (HDM) is one of the most common allergens. However, the role of IL-23 in HDM-induced mouse model is not well understood.
Objective:To evaluate roles of IL-23 in HDM-induced allergic asthma model, particularly during the allergen sensitization period
Methods: BALB/c mice were repeatedly administered with HDM intra-nasally, to develop acute allergic asthma model. Anti-IL-23p19 antibody was given during HDM sensitization period. And we analyzed the activation of DC in LDLN after last sensitization. In addition, to evaluate the roles of IL-23 at bronchial epithelium contacted with HDM, in vitro BEAS-2B cell experiments were done with HDM stimulation and/or anti-IL23 antibody treatment.
Results: Anti-IL-23 antibody treatment during allergen sensitization significantly diminished several phenotypes of allergic asthma; particularly, eosinophilic inflammation and airway hyperresponsiveness were markedly reduced. In bronchoalveolar lavage fluid, IL-4, IL-5, and IL-17A cytokine levels were significantly reduced in anti-IL-23 antibody treated mice. And the activation of DC in LDLN was significantly reduced by anti-IL-23 after last sensitization. In in vitro study, anti-IL-23 treatment prevented pro-inflammatory and pro-allergic cytokine responses in HDM-stimulated BEAS-2B cells.
Conclusion: IL-23 may play a significant role in allergic asthma during allergen sensitization period. Particularly, it may be significantly involved in allergen-contacted epithelial cell responses finally leading to allergic sensitization.
