Evidence map›Paper›PMID 12972516›Full record

ReviewJournal of leukocyte biology2004

Host defense function of the airway epithelium in health and disease: clinical background.

Simon D Message, Sebastian L Johnston

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Viruses in bronchiectasis.ERJ open research · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Phosphocholine-Modified Lipooligosaccharides ofMolecules (Basel, Switzerland) · 2018
    Article
  16. Article
  17. Article
  18. β2-Adrenergic agonists attenuate organic dust-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  19. Article
  20. Review
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 at 1 institution in 1 country.

Simon D MessageDepartment of Respiratory Medicine, Imperial College School of Medicine at St. Mary's, Norfolk Place, London W2 1PG, UK. s.message@imperial.ac.uk
Sebastian L Johnston
Imperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory infection is extremely common and a major cause of morbidity and mortality worldwide. The airway epithelium has an important role in host defense against infection and this is illustrated in this review by considering infection by respiratory viruses. In patients with asthma or chronic obstructive pulmonary disease, respiratory viruses are a common trigger of exacerbations. Rhinoviruses (RV) are the most common virus type detected. Knowledge of the immunopathogenesis of such RV-induced exacerbations remains limited, but information is available from in vitro and from in vivo studies, especially of experimental infection in human volunteers. RV infects and replicates within epithelial cells (EC) of the lower respiratory tract. EC are an important component of the innate-immune response to RV infection. The interaction between virus and the intracellular signaling pathways of the host cell results in activation of potentially antiviral mechanisms, including type 1 interferons and nitric oxide, and in the production of cytokines and chemokines [interleukin (IL)-1 beta, IL-6, IL-8, IL-11, IL-16, tumor necrosis factor alpha, granulocyte macrophage-colony stimulating factor, growth-regulated oncogene-alpha, epithelial neutrophil-activating protein-78, regulated on activation, normal T expressed and secreted, eotaxin 1/2, macrophage-inflammatory protein-1 alpha], which influence the subsequent induced innate- and specific-immune response. Although this is beneficial in facilitating clearance of virus from the respiratory tract, the generation of proinflammatory mediators and the recruitment of inflammatory cells result in a degree of immunopathology and may amplify pre-existing airway inflammation. Further research will be necessary to determine whether modification of EC responses to respiratory virus infection will be of therapeutic benefit.

Indexed as

AdultAsthmaChemokinesChildCytokinesHumansInfantReference ValuesRespiratory MucosaRespiratory Tract DiseasesVirus DiseasesChemokinesCytokines

Identifiers

PMID12972516
PMCPMC7167170
OpenAlexW2084684444

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.