Evidence map›Paper›PMID 28730605›Full record

ArticleImmunity, inflammation and disease2017

Contributions of Interleukin-33 and TSLP in a papain-soaked contact lens-induced mouse conjunctival inflammation model.

Jobu Sugita, Yosuke Asada, Waka Ishida, Satoshi Iwamoto, Katsuko Sudo, Hajime Suto, Toru Matsunaga, Ken Fukuda, Atsuki Fukushima, Norihiko Yokoi and 7 more

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2017. 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
1.0field-weighted citation impact, top 26% 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, 25 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. ILCs and Allergy.Advances in experimental medicine and biology · 2022
    Article
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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

17 authors at 8 institutions in 2 countries.

Jobu SugitaLaboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan.
Yosuke AsadaLaboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan.
Waka IshidaDepartment of Ophthalmology, Kochi University School of Medicine, Nankoku, Japan.
Satoshi IwamotoLaboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan.
Katsuko SudoAnimal Research Center, Tokyo Medical University, Tokyo, Japan.
Hajime SutoDepartment of Dermatology, Juntendo University School of Medicine, Tokyo, Japan.
Toru MatsunagaLaboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan.
Ken FukudaDepartment of Ophthalmology, Kochi University School of Medicine, Nankoku, Japan.
Atsuki FukushimaDepartment of Ophthalmology, Kochi University School of Medicine, Nankoku, Japan.
Norihiko YokoiDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tatsukuni OhnoDepartment of Allergy and Immunology, Department of Molecular Immunology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan.
Miyuki AzumaDepartment of Allergy and Immunology, Department of Molecular Immunology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan.
Nobuyuki EbiharaLaboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan.
Hirohisa SaitoNational Research Institute for Child Health and Development, Tokyo, Japan.
Masato KuboDivision of Molecular Pathology, Research Institute for Biological Sciences, Tokyo University of Sciences, Chiba, Japan.
Susumu NakaeJapan Frontier Research Initiative, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Akira MatsudaLaboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan.ORCID 0000-0002-0792-3663
Juntendo University · JPKōchi University · JPTokyo University of Science · JPTokyo Medical and Dental University · JPKyoto Prefectural University of Medicine · JPNational Center For Child Health and Development · JPTokyo Medical University · JPTokyo University of Information Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPathological changes of severe chronic allergic conjunctivitis are driven not only via acquired immunity but also via innate immunity. Type 2 immune response-initiating cytokines may play some roles as innate immunity-dependent components of the ocular surface inflammation. To investigate the involvement of type 2 immune response-initiating cytokines in innate immunity-dependent, papain-induced conjunctival inflammation model using IL-25-, IL-33-, and TSLP receptor (TSLPR)-knockout (KO) mice with reference to basophils and ILC2.

methodsPapain-soaked contact lenses (papain-CLs) were installed in the conjunctival sacs of C57BL/6-IL-25 KO, IL-33 KO, TSLPR KO, Rag2 KO, Bas-TRECK, and wild-type mice and their eyes were sampled at day 5. The eosinophil and basophil infiltration in papain-CL model was evaluated histologically and cytokine expression was examined. To clarify the roles of basophils and ILC2, basophil/ILC2-depletion experiments were carried out.

resultsPapain-induced conjunctival inflammation exhibited eosinophil infiltration and upregulation of Th2 cytokine expression. Reduction of eosinophil and basophil infiltration and attenuated Th2 cytokine expression were observed in the papain-CL model using IL-33 KO and TSLPR KO mice. Depletion of basophils or ILC2s in the conjunctivae of the papain-CL model reduced eosinophil infiltration.

conclusionsInnate immunity-driven type 2 immune responses of the ocular surface are dependent on IL-33, TSLP, basophils, and ILC2. These components may be possible therapeutic targets for refractory allergic keratoconjunctivitis.

Indexed as

AnimalsBasophilsBiomarkersConjunctivitis, AllergicContact LensesCytokinesDisease Models, AnimalInflammation MediatorsInterleukin-33MiceMice, KnockoutPapainThymic Stromal LymphopoietinBiomarkersCytokinesInflammation MediatorsInterleukin-33PapainThymic Stromal LymphopoietinTSLP protein, mouseBasophilIL-33ILC2papain-induced conjunctivitisTSLP

Identifiers

PMID28730605
PMCPMC5691312
OpenAlexW2737345064

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.