Evidence map›Paper›PMID 28583446›Full record

ReviewThe Journal of allergy and clinical immunology2017

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients.

Matthew Loxham, Donna E Davies

Abstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Amelioration of Inflammation in Rats with Experimentally Induced Asthma byInternational journal of molecular sciences · 2024
    Article
  8. Article
  9. Review
  10. The epithelial era of asthma research: knowledge gaps and future direction for patient care.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  11. Bacteria and Allergic Diseases.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. 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

2 authors.

Matthew LoxhamClinical and Experimental Sciences and the Southampton NIHR Respiratory Biomedical Research Unit, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories, University Hospital Southampton, Southampton, United Kingdom.
Donna E DaviesClinical and Experimental Sciences and the Southampton NIHR Respiratory Biomedical Research Unit, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories, University Hospital Southampton, Southampton, United Kingdom. Electronic address: donnad@soton.ac.uk.

Funding

Medical Research Council G0800766Medical Research Council G0900453National Centre for the Replacement, Refinement and Reduction of Animals in Research G1001598/1
6 · The paper itself

Abstract

The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation.

Indexed as

AnimalsAsthmaGenetic Predisposition to DiseaseHumansPhenotypeRespiratory MucosaAsthmacytokinehomeostasisinnate immunitytight junction

Identifiers

PMID28583446
PMCPMC5457128

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.