Evidence map›Paper›PMID 15005746›Full record

ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2004

Prolonged allergen challenge in mice leads to persistent airway remodelling.

S J McMillan, C M Lloyd

Abstract read
In one paragraph

Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
–field-weighted citation impact
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

91 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Characterization of Lung Inflammatory Response toJournal of fungi (Basel, Switzerland) · 2023
    Article
  6. Review
  7. The RNA binding proteinsFrontiers in cell and developmental biology · 2023
    Article
  8. Article
  9. Ozone in the Development of Pediatric Asthma and Atopic Disease.Immunology and allergy clinics of North America · 2022
    Review
  10. Lung Regeneration: Cells, Models, and Mechanisms.Cold Spring Harbor perspectives in biology · 2022
    Review
  11. Systemic administration of c-KitBMC molecular and cell biology · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. High dose vitamin DScientific reports · 2020
    Article
  18. Article
  19. Article
  20. Article

31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

S J McMillanLeukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College, London, UK.
C M Lloyd

Funding

Wellcome Trust 057704Wellcome Trust 087618
6 · The paper itself

Abstract

backgroundInflammatory infiltrates, airway hyper-responsiveness, goblet cell hyperplasia and subepithelial thickening are characteristic of chronic asthma. Current animal models of allergen-induced airway inflammation generally concentrate on the acute inflammation following allergen exposure and fail to mimic all of these features.

objectiveThe aim of this study was to use a murine model of prolonged allergen-induced airway inflammation in order to characterize the cells and molecules involved in the ensuing airway remodelling. Moreover, we investigated whether remodelling persists in the absence of continued allergen challenge.

methodsAcute pulmonary eosinophilia and airways hyper-reactivity were induced after six serial allergen challenges in sensitized mice (acute phase). Mice were subsequently challenged three times a week with ovalbumin (OVA) (chronic phase) up to day 55. To investigate the persistence of pathology, one group of mice were left for another 4 weeks without further allergen challenge (day 80).

resultsThe extended OVA challenge protocol caused significant airway remodelling, which was absent in the acute phase. Specifically, remodelling was characterized by deposition of collagen as well as airway smooth muscle and goblet cell hyperplasia. Importantly, these airway changes, together with tissue eosinophilia were sustained in the absence of further allergen challenge. Examination of cytokines revealed a dramatic up-regulation of IL-4 and tumour growth factor-beta1 during the chronic phase. Interestingly, while IL-4 levels were significantly increased during the chronic phase, levels of IL-13 fell. Levels of the Th1-associated cytokine IFN-gamma also increased during the chronic phase.

conclusionIn conclusion, we have demonstrated that prolonged allergen challenge results in persistent airway wall remodelling.

Indexed as

AllergensOvalbuminAcute DiseaseAnimalsAsthmaBronchial Provocation TestsBronchoalveolar Lavage FluidChronic DiseaseCollagenFemaleGoblet CellsHyperplasiaInterferon-gammaInterleukin-13Interleukin-4MiceAllergensCollagenInterferon-gammaInterleukin-13Interleukin-4OvalbuminTransforming Growth Factor beta

Identifiers

PMID15005746
PMCPMC3428844

What OpenQuestion holds

Textmetadata
LicenceTDM
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.