Evidence map›Paper›PMID 40644479›Full record

ArticleInternational forum of allergy & rhinology2025

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

Miran Kang, Yohan Seo, Ju Hee Seo, Yeonsu Jeong, Hyejin Jeon, Su-Myeong Jang, Chang-Hoon Kim, Wan Namkung, Hyung-Ju Cho

Abstract read
In one paragraph

Article in International forum of allergy & rhinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Miran KangDepartment of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, South Korea.
Yohan SeoCollege of Pharmacy, Yonsei Institute of Pharmaceutical Science, Yonsei University, Incheon, South Korea.
Ju Hee SeoDepartment of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, South Korea.
Yeonsu JeongDepartment of Otorhinolaryngology-Head and Neck Surgery, Chung-Ang University College of Medicine, Seoul, South Korea.
Hyejin JeonCollege of Pharmacy, Yonsei Institute of Pharmaceutical Science, Yonsei University, Incheon, South Korea.
Su-Myeong JangCollege of Pharmacy, Yonsei Institute of Pharmaceutical Science, Yonsei University, Incheon, South Korea.
Chang-Hoon KimDepartment of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, South Korea.ORCID 0000-0003-1238-6396
Wan NamkungCollege of Pharmacy, Yonsei Institute of Pharmaceutical Science, Yonsei University, Incheon, South Korea.
Hyung-Ju ChoDepartment of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, South Korea.ORCID 0000-0002-2851-3225

Funding

Korean government (MSIT) NRF-2018R1A6A1A03023718Korean government (MSIT) NRF-2021R1A2C2010811Korean government (MSIT) NRF-2022M3A9J4079468Korean government (MSIT) RS-2023-00220853National Research Foundation of Korea"Team Science Award" of Yonsei University College of Medicine 6-2021-0005
6 · The paper itself

Abstract

backgroundAllergic 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.

objectiveThis 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.

methodsWe 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.

resultsIn 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.

conclusionsSelective 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.

Indexed as

AsthmaReceptor, PAR-2Rhinitis, AllergicTh1 CellsTh2 CellsAnimalsCells, CulturedCytokinesDisease Models, AnimalEpithelial CellsHumansMiceMice, KnockoutNasal MucosaPyroglyphidaeSignal TransductionCytokinesReceptor, PAR-2allergic airway inflammationprotease‐activated receptor 2punicalaginrhinitis and asthmaTh1/Th2 responses

Identifiers

PMID40644479
PMCPMC12676653

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.