Evidence map›Paper›PMID 30402955›Full record

ArticleAllergy2019

Chitinase 3-like 1 protein plays a critical role in respiratory syncytial virus-induced airway inflammation.

Min Jung Kim, Doo Hee Shim, Hye-Ran Cha, Kuk-Young Moon, Chang Mo Yang, Su Jin Hwang, Kyung Won Kim, Jeon Han Park, Chun Geun Lee, Jack A Elias and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Allergy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Potential role of chitinase-3-like protein 1 (CHI3L1/YKL-40) in neurodegeneration and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
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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

12 authors at 2 institutions in 2 countries.

Min Jung KimDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-5634-9709
Doo Hee ShimDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-6696-7199
Hye-Ran ChaDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0001-7112-7525
Kuk-Young MoonDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Chang Mo YangDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Su Jin HwangDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Kyung Won KimDepartment of Pediatrics, Severance Hospital, Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0003-4529-6135
Jeon Han ParkDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0001-9604-3205
Chun Geun LeeDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island, USA.ORCID 0000-0002-9514-3658
Jack A EliasDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island, USA.
Myung Hyun SohnDepartment of Pediatrics, Severance Hospital, Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-2478-487X
Jae Myun LeeDepartment of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-5273-3113
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
Korea Health Industry Development Institute HI13C0826Korea Health Industry Development Institute HI15C2971Korea Health Industry Development Institute HI17C0104National Research Foundation of Korea NRF-2017R1A2B2004043NHLBI NIH HHS P01 HL114501
6 · The paper itself

Abstract

backgroundChitinase 3-like 1 protein (CHI3L1) (YKL-40 in humans and breast regression protein [BRP]-39 in mice) is required for optimal allergen sensitization and Th2 inflammation in various chronic inflammatory diseases including asthma. However, the role of CHI3L1 in airway inflammation induced by respiratory viruses has not been investigated. The aim of this study was to investigate the relationship between CHI3L1 and airway inflammation caused by respiratory syncytial virus (RSV) infection.

methodsWe measured YKL-40 levels in human nasopharyngeal aspirate (NPA) from hospitalized children presenting with acute respiratory symptoms. Wild-type (WT) and BRP-39 knockout (KO) C57BL/6 mice were inoculated with live RSV (A2 strain). Bronchoalveolar lavage fluid and lung tissue samples were obtained on day 7 after inoculation to assess lung inflammation, airway reactivity, and expression of cytokines and BRP-39.

resultsIn human subjects, YKL-40 and IL-13 levels in NPA were higher in children with RSV infection than in control subjects. Expression of BRP-39 and Th2 cytokines, IL-13 in particular, was increased following RSV infection in mice. Airway inflammation caused by RSV infection was reduced in BRP-39 KO mice as compared to WT mice. Th2 cytokine levels were not increased in the lungs of RSV-infected BRP-39 KO mice. BRP-39 regulated M2 macrophage activation in RSV-infected mice. Additionally, treatment with anti-CHI3L1 antibody attenuated airway inflammation and Th2 cytokine production in RSV-infected WT mice.

conclusionThese findings suggest that CHI3L1 could contribute to airway inflammation induced by RSV infection. CHI3L1 could be a potential therapeutic candidate for attenuating Th2-associated immunopathology during RSV infection.

Indexed as

AnimalsAsthmaCase-Control StudiesChildChitinase-3-Like Protein 1CytokinesFemaleGrowth SubstancesHumansInflammationMiceMice, Inbred C57BLRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsRespiratory SystemCHI3L1 protein, humanChil1 protein, mouseChitinase-3-Like Protein 1CytokinesGrowth Substancesbronchiolitischitinase 3-like 1 proteinlower respiratory tract infectionrespiratory syncytial virusestype 2 immunity

Identifiers

PMID30402955
PMCPMC7159489
OpenAlexW2900221198

What OpenQuestion holds

Textmetadata
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.