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Selective PAR2 Inhibition Attenuates HDM-Induced Th1/Th2 Responses in Human Epithelial and Murine Models of Allergic Rhinitis and Asthma

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dc.contributor.author김창훈-
dc.contributor.author조형주-
dc.date.accessioned2025-10-15T01:37:22Z-
dc.date.available2025-10-15T01:37:22Z-
dc.date.issued2025-07-
dc.identifier.issn2042-6976-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/207428-
dc.description.abstractTh1/Th2 responses; allergic airway inflammation; protease‐activated receptor 2; punicalagin; rhinitis and asthma-
dc.description.statementOfResponsibilityhttps://onlinelibrary.wiley.com/doi/full/10.1002/alr.23623-
dc.languageEnglish-
dc.publisherWiley-Blackwell-
dc.relation.isPartOfINTERNATIONAL FORUM OF ALLERGY & RHINOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESH1-
dc.titleSelective PAR2 Inhibition Attenuates HDM-Induced Th1/Th2 Responses in Human Epithelial and Murine Models of Allergic Rhinitis and Asthma-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Otorhinolaryngology (이비인후과학교실)-
dc.contributor.googleauthorMiran Kang-
dc.contributor.googleauthorYohan Seo-
dc.contributor.googleauthorJu Hee Seo-
dc.contributor.googleauthorYeonsu Jeong-
dc.contributor.googleauthorHyejin Jeon-
dc.contributor.googleauthorSu-Myeong Jang-
dc.contributor.googleauthorChang-Hoon Kim-
dc.contributor.googleauthorWan Namkung-
dc.contributor.googleauthorHyung-Ju Cho-
dc.identifier.doiBackground: Allergic rhinitis (AR) and asthma are involved in complex interactions between Th1 and Th2 inflammatory pathways. House dust mite (HDM) activates protease-activated receptor 2 (PAR2) to trigger inflammatory responses, but current treatments often provide inadequate control. Objective: This study aimed to investigate the effects of selective PAR2 inhibition on Th1 and Th2 responses in human nasal epithelial (HNE) cells and murine models of AR and asthma. Methods: We examined the effects of selective PAR2 inhibition using primary HNE cells and HDM-induced mouse models (PAR2-wild-type [PAR2-wt] and knockout [PAR2-ko]). Analyses included inflammatory signaling pathways, cytokine profiles, airway responses, histopathology, and transcriptomics. Results: In HNE cells, PAR2 inhibition suppressed Th2 (interleukin [IL]-33, TSLP) and Th1 (TNF-α, IL-6) inflammatory cytokines while inhibiting calcium mobilization and ERK/NF-κB signaling cascades. In PAR2-wt mice, treatment with the PAR2 inhibitor reduced HDM-specific Immunoglobulin E (IgE), airway hyperresponsiveness, and allergic inflammation in both nasal and bronchial tissues, matching the anti-inflammatory profile of PAR2-ko mice. Bulk RNA sequencing confirmed comprehensive suppression of inflammatory gene expression. Conclusions: Selective PAR2 inhibition effectively attenuates HDM-induced allergic inflammation by modulation of Th1 and Th2 pathways in human airway epithelium and murine models. We suggest that PAR2 can be a possible target for AR and asthma.-
dc.contributor.localIdA01050-
dc.contributor.localIdA03936-
dc.relation.journalcodeJ03004-
dc.identifier.eissn2042-6984-
dc.identifier.pmid40644479-
dc.contributor.alternativeNameKim, Chang Hoon-
dc.contributor.affiliatedAuthor김창훈-
dc.contributor.affiliatedAuthor조형주-
dc.citation.volume11-
dc.citation.startPagee23623-
dc.identifier.bibliographicCitationINTERNATIONAL FORUM OF ALLERGY & RHINOLOGY, Vol.11 : e23623, 2025-07-
dc.identifier.articleno10.1002/alr.23623-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
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