Hyun Seung Lee
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Da-Eun Park
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Boram Bae
,
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
Mingyu Kang, MD
,
Internal Medicine, Subdivision of Allergy, Chungbuk National University Hospital, Cheongju, South Korea
Han-Ki Park, MD
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, 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
Hye-Young Kim
,
Department of Pediatrics, Medical Research Institute of Pusan National University Hospital, Busan, South Korea
Kyung-up Min, MD, PhD
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Sang-Heon Cho, MD, PhD
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Ji-Won Lee
,
Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea
Background: Recently, it has been reported that cigarette smoke exposure during allergen sensitization period facilitates the development of house dust mite (HDM) sensitization and subsequent allergic asthma. However, the mechanisms remain elusive. Several researchers have recently shown that IL-23 is involved in antigen-induced airway inflammation. Therefore, we hypothesized that IL-23 is involved in this pathway.
Objective: To evaluate roles of IL-23 in short cigarette smoke exposure-induced HDM-allergic asthma mouse model
Methods: BALB/c mice were exposed to HDM and/or cigarette smoke extracts (CSE) during HDM sensitization period (day 1, 2, 3, and 14). Anti-IL-23p19 antibody was given during the sensitization period. And we analyzed several asthmatic phenotypes after last allergen challenge. In addition, we also analyzed the change of DC activation in LDLN and cytokines profile after last sensitization.
Results: CSE exposure during sensitization period promoted the development of HDM-allergic sensitization and asthma phenotypes. The proportion of innate lymphoid type 2 cells also increased by CSE and HDM co-exposure, compared to a single exposure. Anti-IL-23 antibody treatment during allergen sensitization period significantly diminished several phenotypes of allergic asthma. Anti-IL-23 treatment also reduced the recruitment of innate lymphoid type 2 cells. Along with, the activation of DC in LDLN was significantly reduced by anti-IL-23 after last sensitization.
Conclusion: IL-23 may play a significant role in the development of short cigarette smoke-induced allergic sensitization and asthma.
