Ha-Jung Kim
,
Asan Institute for Life Sciences, Seoul, South Korea
Young-Joon Kim
,
Asan Institute for Life Sciences, Seoul, South Korea
Bok Kyoung Jung
,
Asan Institute for Life Sciences, Seoul, South Korea
Seung-Hwa Lee
,
Asan Institute for Life Sciences, Seoul, South Korea
Mi-Jin Kang, MS
,
Asan Institute for Life Sciences, Seoul, South Korea
Sekyoo Jeong
,
Neopharm Co., Ltd, Seoul, South Korea
Eun Lee, MD
,
Asan Medical Center, Seoul, South Korea
Hyun-Ju Cho, MD
,
Department of Pediatrics, Childhood Asthma Atopy Center, Enviromental Health Center, University of Ulsan College of Medicine,, Asan Medical Center, Seoul, South Korea
Young-Ho Kim, MD
,
Department of Pediatrics, Childhood Asthma Atopy Center, Enviromental Health Center, University of Ulsan College of Medicine,, Asan Medical Center, Seoul, South Korea
Song-I Yang, MD
,
Department of Pediatrics, Hallym University Sacred Heart Hospital, Anyang, South Korea
Seo Hee Kim
,
Asan Medical Center, Seoul, South Korea
Soo-Jong Hong, MD, PhD
,
Department of Pediatrics, Childhood Asthma Atopy Center, Enviromental Health Center, University of Ulsan College of Medicine,, Asan Medical Center, Seoul, South Korea
Background: Protease in the common allergens (e.g., cockroach, mold) can induce a pathogenesis on allergic diseases. Protease activated receptor 2 (PAR2) is reported to trigger immune response on allergic asthma.
Aim: This study aimed to investigate the effects of a PAR2-antagonist on protease-induced allergic inflammation and identify the mechanism.
Methods: PAR2-antagonist was administered intranasally in the mouse model of asthma induced by German cockroach extract (GCE). In addition, human lung epithelial cells (A549 cells) were treated with GCE, PAR2-antagonist, and NAC to confirm the mechanism related in the vivo results.
Results: Airway hyperresponsiveness, total IgE production, and pulmonary inflammation were significantly suppressed by NAC and the PAR2-antagonist in the mouse model. Th2-cytokines and TSLP in the lung were suppressed by the NAC and PAR-2 antagonist. Tight junction protein, claudin-1 was disturbed by GCE and restored by PAR2-antagonist and NAC in the lung. TSLP and claudin-1 showed the same correlation in the human lung epithelial cells by the two in vitro.
Conclusions: GCE elicits allergic inflammation mediated by disruption of tight junction triggered by PAR2 and generation of ROS.
