Evidence map›Paper›PMID 31172724›Full record

ArticleAllergy, asthma & immunology research2019

Protease-Activated Receptors 2-Antagonist Suppresses Asthma by Inhibiting Reactive Oxygen Species-Thymic Stromal Lymphopoietin Inflammation and Epithelial Tight Junction Degradation.

Ha Jung Kim, Seung Hwa Lee, Sekyoo Jeong, Soo Jong Hong

Open access · bronzeAbstract read
In one paragraph

Article in Allergy, asthma & immunology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  8. Lipopeptide Pepducins as Therapeutic Agents.Methods in molecular biology (Clifton, N.J.) · 2022
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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

4 authors at 3 institutions in 1 country.

Ha Jung KimDepartment of Internal Medicine, Chonnam National University College of Veterinary Medicine, Gwangju, Korea.ORCID https://orcid.org/0000-0002-2699-0263
Seung Hwa LeeAsan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-9359-0318
Sekyoo JeongCRID Center, NeoPharm Co., Ltd., Daejeon, Korea.ORCID https://orcid.org/0000-0002-9201-0227
Soo Jong HongDepartment of Pediatrics, Childhood Asthma Atopy Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0003-1409-2113
Ulsan College · KRChonnam National University · KRKomipharm International (South Korea) · KR

Funding

Ministry of Health and Welfare HI13C1674
6 · The paper itself

Abstract

purposeProtease-activated receptor 2 (PAR2) reportedly triggers the immune response in allergic asthma. We aimed to investigate the mechanism on allergic inflammation mediated by PAR2.

methodsHuman lung epithelial cells (A549 cells) were used for

resultsIn A549 cells, the levels of reactive oxygen species (ROS) and thymic stromal lymphopoietin (TSLP) were significantly increased by GCE treatment, but were suppressed by PAR2-antagonist (PAR2-ant) or N-acetylcysteine (NAC) treatment. Claudin-1 was degraded by GCE, and was restored by PAR2-ant or NAC in the cells. In the mouse model, the clinical appearance including bronchial hyperresponsiveness, bronchoalveolar lavage fluid analysis and total immunoglobulin E were significantly suppressed by PAR2-ant or NAC. Moreover, TSLP levels in the lung were suppressed by the same treatments in the lung. Claudin-1 was also degraded by GCE, and was restored by PAR2-ant or NAC.

conclusionsROS generation and epidermal tight junction degradation are triggered by protease, followed by the induction of TSLP in allergic asthma. Our findings could suggest that PAR2-ant or anti-oxidants could be considered for allergic diseases as preventive alternatives.

Indexed as

Asthmaprotease-activated receptor 2reactive oxygen speciesthymic stromal lymphopoietintight junction

Identifiers

PMID31172724
PMCPMC6557777
OpenAlexW2949505988

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.