Evidence map›Paper›PMID 25807992›Full record

ArticleImmunology2015

Distinct sustained structural and functional effects of interleukin-33 and interleukin-25 on the airways in a murine asthma surrogate.

Yan Li, Wei Wang, Ping Huang, Qian Zhang, Xiujuan Yao, Jingjing Wang, Zhe Lv, Yunqing An, Chris J Corrigan, Kewu Huang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Glucocorticoid Receptor Binding Inhibits an IntronicInternational journal of molecular sciences · 2018
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. IL-33 Signaling in Lung Injury.Translational perioperative and pain medicine · 2016
    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

11 authors at 3 institutions in 2 countries.

Yan LiThe Department of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University & Beijing Institute of Respiratory Medicine, Beijing, China.
Wei WangThe Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Ping HuangThe Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Qian ZhangThe Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing.
Xiujuan YaoThe Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing.
Jingjing WangThe Department of Laboratory Animal Sciences, Capital Medical University, Beijing, China.
Zhe LvThe Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yunqing AnThe Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Chris J CorriganDivision of Asthma, Allergy & Lung Biology, MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, King's College London, London, UK.
Kewu HuangThe Department of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University & Beijing Institute of Respiratory Medicine, Beijing, China.
Sun YingThe Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Capital Medical University · CNBeijing Tongren Hospital · CNKing's College London · GB

Funding

Medical Research Council G1000758
6 · The paper itself

Abstract

Interleukin-25 (IL-25) and IL-33, which belong to distinct cytokine families, induce and promote T helper type 2 airway inflammation. Both cytokines probably play a role in asthma, but there is a lack of direct evidence to clarify distinctions between their functions and how they might contribute to distinct 'endotypes' of disease. To address this, we made a direct comparison of the effects of IL-25 and IL-33 on airway inflammation and physiology in our established murine asthma surrogate, which involves per-nasal, direct airway challenge. Intranasal challenge with IL-33 or IL-25 induced inflammatory cellular infiltration, collagen deposition, airway smooth muscle hypertrophy, angiogenesis and airway hyper-responsiveness, but neither increased systemic production of IgE or IgG1. Compared with that of IL-25, the IL-33-induced response was characterized by more sustained laying down of extracellular matrix protein, neoangiogenesis, T helper type 2 cytokine expression and elevation of tissue damping. Hence, both IL-25 and IL-33 may contribute significantly and independently to asthma 'endotypes' when considering molecular targets for the treatment of human disease.

Indexed as

AnimalsAsthmaDisease Models, AnimalExtracellular Matrix ProteinsHumansImmunoglobulin EImmunoglobulin GInterleukin-33InterleukinsMiceMice, Inbred BALB CTh2 CellsExtracellular Matrix ProteinsIl33 protein, mouseImmunoglobulin EImmunoglobulin GInterleukin-33InterleukinsMydgf protein, mouseasthmainterleukin-25interleukin-33remodelling

Identifiers

PMID25807992
PMCPMC4515131
OpenAlexW2137283203

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.