Evidence map›Paper›PMID 26428949›Full record

ArticleInternational immunology2016

Murine allergic rhinitis and nasal Th2 activation are mediated via TSLP- and IL-33-signaling pathways.

Shoko Akasaki, Kazufumi Matsushita, Yukinori Kato, Ayumi Fukuoka, Naruhito Iwasaki, Masakiyo Nakahira, Shigeharu Fujieda, Koubun Yasuda, Tomohiro Yoshimoto

Open access · greenAbstract read
In one paragraph

Article in International immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. The role of the CBM complex in allergic inflammation and disease.The Journal of allergy and clinical immunology · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Mechanisms of Allergen Immunotherapy in Allergic Rhinitis.Current allergy and asthma reports · 2020
    Review
  11. [Advances of IL-33/ST2 signaling pathway in allergic rhinitis].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Interleukin-33: Its Emerging Role in Allergic Diseases.Molecules (Basel, Switzerland) · 2018
    Review
  17. Article
  18. Article
  19. The Role of the Sinonasal Epithelium in Allergic Rhinitis.Otolaryngologic clinics of North America · 2017
    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

9 authors at 2 institutions in 1 country.

Shoko AkasakiLaboratory of Allergic Diseases, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Kazufumi MatsushitaLaboratory of Allergic Diseases, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Yukinori KatoLaboratory of Allergic Diseases, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan Department of Otorhinolaryngology-Head and Neck Surgery, Faculty of Medical Science, University of Fukui, Fukui 910-1193, Japan.
Ayumi FukuokaLaboratory of Allergic Diseases, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Naruhito IwasakiLaboratory of Allergic Diseases, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan Department of Otorhinolaryngology, Shiga University of Medical Science, Otsu, Shiga 520-2121, Japan.
Masakiyo NakahiraDepartment of Immunology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Shigeharu FujiedaDepartment of Otorhinolaryngology-Head and Neck Surgery, Faculty of Medical Science, University of Fukui, Fukui 910-1193, Japan.
Koubun YasudaDepartment of Immunology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Tomohiro YoshimotoLaboratory of Allergic Diseases, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan Department of Immunology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan tomo@hyo-med.ac.jp.
Hyogo Medical University · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thymic stromal lymphopoietin (TSLP) and IL-33 are epithelium-derived proallergic cytokines that contribute to allergic diseases. Although the involvement of TSLP in allergic rhinitis (AR) is suggested, the exact role of TSLP in AR is poorly understood. Furthermore, the relative contribution of TSLP and IL-33 in nasal allergic responses has not been described. In this study, we examined the roles of TSLP and IL-33 in AR by analyzing acute and chronic AR models. Acute AR mice were intraperitoneally immunized with ragweed, then intranasally challenged with ragweed pollen for four consecutive days. Chronic AR mice were nasally administrated ragweed pollen on consecutive days for 3 weeks. In both models, TSLP receptor (TSLPR)-deficient mice showed defective sneezing responses and reduced serum ragweed-specific IgE levels compared with wild-type (WT) mice. Analyses of bone-marrow chimeric mice demonstrated that hematopoietic cells were responsible for defective sneezing in TSLPR-deficient mice. In addition, FcεRI(+)-cell-specific TSLPR-deficient mice showed partial but significant reduction in sneezing responses. Of note, Th2 activation and nasal eosinophilia were comparable between WT and TSLPR-deficient mice. ST2- and IL-33-deficient mice showed defective Th2 activation and nasal eosinophilia to acute, but not chronic, ragweed exposure. TSLPR and ST2 double-deficient mice showed defective Th2 activation and nasal eosinophilia even after chronic ragweed exposure. These results demonstrate that TSLPR signaling is critical for the early phase response of AR by controlling the IgE-mast-cell/basophil pathway. The IL-33/ST2 pathway is central to nasal Th2 activation during acute allergen exposure, but both TSLPR and ST2 contribute to Th2 responses in chronically allergen-exposed mice.

Indexed as

Acute DiseaseAllergensAmbrosiaAnimalsAntigens, PlantChronic DiseaseCytokinesHumansImmunoglobulinsInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MiceMice, Inbred BALB CMice, KnockoutNasal MucosaPollenAllergensAntigens, PlantCytokinesFcepsilonRIalpha protein, mouseIl1rl1 protein, mouseImmunoglobulinsInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Receptors, CytokineReceptors, IgEThymic Stromal LymphopoietinTslpr protein, mouseimmunoglobulin Einterleukin-33mast cellsnosethymic stromal lymphopoietin

Identifiers

PMID26428949
PMCPMC4885219
OpenAlexW2267504684

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.