Evidence map›Paper›PMID 30082755›Full record

ArticleScientific reports2018

Chitin promotes antigen-specific Th2 cell-mediated murine asthma through induction of IL-33-mediated IL-1β production by DCs.

Ken Arae, Hideaki Morita, Hirotoshi Unno, Kenichiro Motomura, Sumika Toyama, Naoko Okada, Tatsukuni Ohno, Masato Tamari, Keisuke Orimo, Yuko Mishima and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
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  4. Article
  5. Fungal chitin is not an independent mediator of allergic fungal asthma severity.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  6. Article
  7. Long-term exposure to house dust mites accelerates lung cancer development in mice.Journal of experimental & clinical cancer research : CR · 2023
    Article
  8. Chitinase-3-like 1 regulates TFrontiers in immunology · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. FSTL1 aggravates OVA-induced inflammatory responses by activating the NLRP3/IL-1β signaling pathway in mice and macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  13. Article
  14. Article
  15. Review
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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

18 authors at 6 institutions in 1 country.

Ken AraeDepartment of Immunology, Faculty of Health Sciences, Kyorin University, Tokyo, 181-8612, Japan.
Hideaki MoritaDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Hirotoshi UnnoDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Kenichiro MotomuraDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Sumika ToyamaDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.ORCID 0000-0003-3606-245X
Naoko OkadaDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Tatsukuni OhnoDepartment of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, 113-8510, Japan.
Masato TamariDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Keisuke OrimoDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Yuko MishimaDepartment of Immunology, Faculty of Health Sciences, Kyorin University, Tokyo, 181-8612, Japan.
Hajime SutoAtopy Research Center, Juntendo University, Tokyo, 113-0033, Japan.
Ko OkumuraAtopy Research Center, Juntendo University, Tokyo, 113-0033, Japan.
Katsuko SudoAnimal Research Center, Tokyo Medical University, Tokyo, 160-8402, Japan.
Hiroshi MiyazawaDepartment of Medical technology, Faculty of Health Sciences, Kyorin University, Tokyo, 181-8612, Japan.
Haruhiko TaguchiDepartment of Immunology, Faculty of Health Sciences, Kyorin University, Tokyo, 181-8612, Japan.
Hirohisa SaitoDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Kenji MatsumotoDepartment of Allergy and Clinical Immunology,  National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Susumu NakaeLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan. snakae@ims.u-tokyo.ac.jp.
National Center For Child Health and Development · JPKyorin University · JPJuntendo University · JPJapan Science and Technology Agency · JPTokyo Medical and Dental University · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chitin, which is a major component of house dust mites (HDM), fungi, crustaceans, etc., can activate immune cells, suggesting that it contributes to development of allergic disorders such as asthma. Although the pathophysiological sensitization route of asthmatic patients to allergens is considered via the respiratory tract, the roles of intranasally-administered chitin in development of asthma remain unclear. After ovalbumin (OVA) challenge, development of airway inflammation was profoundly exacerbated in mice sensitized with OVA in the presence of chitin. The exacerbation was dependent on IL-33, but not IL-25, thymic stromal lymphopoietin or IL-17A. Chitin enhanced IL-33-dependent IL-1β production by dendritic cells (DCs). Furthermore, chitin- and IL-33-stimulated DC-derived IL-1β promoted OVA-specific Th2 cell activation, resulting in aggravation of OVA-induced airway inflammation. These findings indicate the adjuvant activity of chitin via a new mechanism and provide important clues for development of therapeutics for allergic disorders caused by HDM, fungi and crustaceans.

Indexed as

AnimalsAsthmaBronchoalveolar LavageChitinDendritic CellsEnzyme-Linked Immunosorbent AssayFemaleInterleukin-1betaInterleukin-33MaleMiceTh2 CellsChitinInterleukin-1betaInterleukin-33

Identifiers

PMID30082755
PMCPMC6079063
OpenAlexW2885773773

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.