Evidence map›Paper›PMID 30575775›Full record

ArticleScientific reports2018

IL-33, IL-25 and TSLP contribute to development of fungal-associated protease-induced innate-type airway inflammation.

Yoshihisa Hiraishi, Sachiko Yamaguchi, Takamichi Yoshizaki, Aya Nambu, Eri Shimura, Ayako Takamori, Seiko Narushima, Wakako Nakanishi, Yosuke Asada, Takafumi Numata and 14 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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
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  4. Mgl2Nature communications · 2025
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  5. Effects ofInternational journal of microbiology · 2025
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  6. PANoptosis opens new treatment options for allergic bronchopulmonary aspergillosis.The journal of allergy and clinical immunology. Global · 2024
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  7. Article
  8. Invariant natural killer T cells in lung diseases.Experimental & molecular medicine · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Immune responses and exacerbations in severe asthma.Current opinion in immunology · 2021
    Review
  19. Innate lymphoid cells are double-edged swords under the mucosal barrier.Journal of cellular and molecular medicine · 2021
    Review
  20. Regulation of Immune Responses by Nonhematopoietic Cells in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
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

24 authors at 10 institutions in 1 country.

Yoshihisa HiraishiLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Sachiko YamaguchiLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Takamichi YoshizakiLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Aya NambuLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.ORCID http://orcid.org/0000-0002-2797-6420
Eri ShimuraLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Ayako TakamoriLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Seiko NarushimaLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Wakako NakanishiLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Yosuke AsadaLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Takafumi NumataLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Maho SuzukawaNational Hospital Organization Tokyo National Hospital, Tokyo, 204-8585, Japan.
Yasuhiro YamauchiDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Akira MatsudaDepartment of Ophthalmology, Juntendo University School of Medicine, Tokyo, 113-8412, Japan.ORCID http://orcid.org/0000-0002-0792-3663
Ken AraeDepartment of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Hideaki MoritaDepartment of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Tomoaki HoshinoThe 1st Department of Medicine, Kurume University School of Medicine, Fukuoka, 830-0011, Japan.
Hajime SutoAtopy Research Center, Juntendo University School of Medicine, Tokyo, 113-8412, Japan.
Ko OkumuraAtopy Research Center, Juntendo University School of Medicine, Tokyo, 113-8412, Japan.
Kenji MatsumotoDepartment of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Hirohisa SaitoDepartment of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.ORCID http://orcid.org/0000-0002-6630-8337
Katsuko SudoAnimal Research Center, Tokyo Medical University, Tokyo, 160-8402, Japan.
Motoyasu IikuraDepartment of Respiratory Medicine, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan.
Takahide NagaseDepartment of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, 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.
Systems Biology Institute · JPJuntendo University · JPNational Center For Child Health and Development · JPThe University of Tokyo · JPJapan Science and Technology Agency · JPJichi Medical University · JPKurume University · JPNational Center for Global Health and Medicine · JPTokyo Medical University · JPTokyo National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Certain proteases derived from house dust mites and plants are considered to trigger initiation of allergic airway inflammation by disrupting tight junctions between epithelial cells. It is known that inhalation of proteases such as house dust mite-derived Der p1 and/or papaya-derived papain caused airway eosinophilia in naïve mice and even in Rag-deficient mice that lack acquired immune cells such as T, B and NKT cells. In contrast, little is known regarding the possible involvement of proteases derived from Aspergillus species (fungal-associated proteases; FAP), which are ubiquitous saprophytic fungi in the environment, in the development of allergic airway eosinophilia. Here, we found that inhalation of FAP by naïve mice led to airway eosinophilia that was dependent on protease-activated receptor-2 (PAR2), but not TLR2 and TLR4. Those findings suggest that the protease activity of FAP, but not endotoxins in FAP, are important in the setting. In addition, development of that eosinophilia was mediated by innate immune cells (ILCs) such as innate lymphoid cells, but not by acquired immune cells such as T, B and NKT cells. Whereas IL-33, IL-25 and thymic stromal lymphopoietin (TSLP) are involved in induction of FAP-induced ILC-mediated airway eosinophilia, IL-33-rather than IL-25 and/or TSLP-was critical for the eosinophilia in our model. Our findings improve our understanding of the molecular mechanisms involved in induction of airway inflammation by FAP.

Indexed as

AllergensAnimalsAspergillusCytokinesImmunity, CellularImmunity, InnateInterleukin-33InterleukinsLung Diseases, FungalMiceMice, Inbred C57BLMice, KnockoutPeptide HydrolasesPneumoniaPulmonary EosinophiliaThymic Stromal LymphopoietinAllergensCytokinesIl33 protein, mouseInterleukin-33InterleukinsMydgf protein, mousePeptide HydrolasesThymic Stromal Lymphopoietin

Identifiers

PMID30575775
PMCPMC6303299
OpenAlexW2904939795

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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.