Evidence map›Paper›PMID 1478679›Full record

ArticleImmunology1992

Expression and generation of interleukin-8, IL-6 and granulocyte-macrophage colony-stimulating factor by bronchial epithelial cells and enhancement by IL-1 beta and tumour necrosis factor-alpha.

O Cromwell, Q Hamid, C J Corrigan, J Barkans, Q Meng, P D Collins, A B Kay

Open access · greenAbstract read
In one paragraph

Article in Immunology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
18.9field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 353 citations in OpenAlex.

  1. Review
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  8. Review
  9. Review
  10. The role of microbiome in rheumatoid arthritis treatment.Therapeutic advances in musculoskeletal disease · 2019
    Review
  11. Article
  12. Lung Defense through IL-8 Carries a Cost of Chronic Lung Remodeling and Impaired Function.American journal of respiratory cell and molecular biology · 2018
    Article
  13. Tight junctions in pulmonary epithelia during lung inflammation.Pflugers Archiv : European journal of physiology · 2017
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

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

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

7 authors at 1 institution in 1 country.

O CromwellDepartment of Allergy and Clinical Immunology, National Heart and Lung Institute, London.
Q Hamid
C J Corrigan
J Barkans
Q Meng
P D Collins
A B Kay
Lung Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have tested the hypothesis that the bronchial epithelium has the capacity to generate and release cytokines that could contribute to inflammatory events associated with inflammatory lung diseases. Messenger RNA (mRNA) for interleukin-6 (IL-6), IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) was identified in human bronchial epithelial cell primary cultures, characterized on the basis of staining for cytokeratin, using both in situ hybridization and Northern blotting. Using in situ hybridization we have shown that the majority of the cells expressed mRNA for IL-6 and IL-8, whereas fewer than 20% of cells expressed message for GM-CSF. The numbers of cells expressing message were increased by culture with tumour necrosis factor-alpha (TNF-alpha) (20 ng/ml, 24 hr). These observations were substantiated by Northern blotting, which showed that both TNF-alpha and IL-1 beta were able to induce a dose-dependent increase in IL-8-specific mRNA. Immunoreactive IL-6 and GM-CSF were detected and quantified in the culture supernatants by ELISA, and IL-8 by radioimmunoassay. The levels of immunoreactivity were increased by incubation of epithelial cells with either IL-1 beta or TNF-alpha for 24 hr. A transformed tracheal epithelial cell line (9HTEo-) expressed mRNA for IL-6, IL-8 and GM-CSF but, whereas levels of immunoreactive IL-6 in culture supernatants were comparable with those in primary cell cultures, levels of IL-8 were low and GM-CSF trivial. These observations indicate that the bronchial epithelium has the potential to be a major source of IL-8 and a number of other cytokines, and that production can be amplified substantially by IL-1 beta and TNF-alpha. The bronchial epithelium is ideally situated to modulate inflammatory and immunological events in and around the airways, and these observations suggest that it could contribute to promote and sustain inflammatory and immunological processes in inflammatory lung diseases such asthma.

Indexed as

Blotting, NorthernBronchiCells, CulturedEpitheliumGranulocyte-Macrophage Colony-Stimulating FactorHumansIn Situ HybridizationInterleukin-1Interleukin-6Interleukin-8Tumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-1Interleukin-6Interleukin-8Tumor Necrosis Factor-alpha

Identifiers

PMID1478679
PMCPMC1421719
OpenAlexW191913208

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.