Evidence map›Paper›PMID 29420850›Full record

ArticleAllergy2018

Chitotriosidase inhibits allergic asthmatic airways via regulation of TGF-β expression and Foxp3

J Y Hong, M Kim, I S Sol, K W Kim, C-M Lee, J A Elias, M H Sohn, C G Lee

Open access · greenAbstract read
In one paragraph

Article in Allergy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Chitinase-3-like 1 regulates TFrontiers in immunology · 2023
    Article
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  15. Review
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  18. Chitotriosidase: a marker and modulator of lung disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

J Y HongDepartment of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
M KimDepartment of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
I S SolDepartment of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
K W KimDepartment of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
C-M LeeMolecular Microbiology and Immunology, Brown University, Providence, RI, USA.
J A EliasMolecular Microbiology and Immunology, Brown University, Providence, RI, USA.
M H SohnDepartment of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-2478-487X
C G LeeMolecular Microbiology and Immunology, Brown University, Providence, RI, USA.ORCID 0000-0002-9514-3658
Yonsei University · KRBrown University · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
YKL-40 in Idiopathic Pulmonary Fibrosis and Kidney TransplantationU01HL108638 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2011 to 2014
$2.6M
Chitinase1 as a Biomarker and Therapeutic Target in Scleroderma Lung DiseaseR01HL115813 · NHLBI · BROWN UNIVERSITY · PI LEE, CHUN GEUN · 2014 to 2017
$1.5M
NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL115813NHLBI NIH HHS U01 HL108638
6 · The paper itself

Abstract

backgroundChitotriosidase (chitinase 1, Chit1), a major true chitinase in humans, is induced in childhood asthma and has been implicated in the pathogenesis of a variety of inflammatory and tissue remodeling responses. However, the role and the mechanisms that underlie these contributions to the diseases have not been defined. We hypothesized that Chit1 plays a significant role in the pathogenesis of allergic asthma.

methodsWild-type and Chit1-deficient mice and cells in culture were used to define the roles of Chit1 in models of allergic adaptive Th2 inflammation. In addition, the levels of sputum Chit1 were evaluated in pediatric asthma patients and compared to control.

resultsThe levels of sputum Chit1 were significantly increased in the patients with childhood asthma. Mice with Chit1 null mutation demonstrated enhanced allergic Th2 inflammatory and cytokine and IgE responses to OVA or house dust mite allergen sensitization and challenge. However, the expression levels of TGF-β1 were significantly decreased with a diminished number of Foxp3

conclusionChit1 plays a protective role in the pathogenesis of allergic inflammation and asthmatic airway responses via regulation of TGF-β expression and Foxp3

Indexed as

Analysis of VarianceAnimalsAsthmaChildChi-Square DistributionDisease Models, AnimalFemaleForkhead Transcription FactorsHexosaminidasesHumansHypersensitivityInterleukin-10Loss of Function MutationMaleMiceMice, Inbred C57BLchitotriosidaseForkhead Transcription FactorsFoxp3 protein, mouseHexosaminidasesIL10 protein, mouseInterleukin-10Transforming Growth Factor beta1asthmachitotriosidaseregulatory T cellTGF-beta1Th2 response

Identifiers

PMID29420850
PMCPMC6047905
OpenAlexW2791304132

What OpenQuestion holds

Textmetadata
LicenceTDM
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.