Evidence map›Paper›PMID 9593769›Full record

ArticleThe Journal of clinical investigation1998

Interleukin (IL) 4 and IL-13 act on human lung fibroblasts. Implication in asthma.

C Doucet, D Brouty-Boyé, C Pottin-Clémenceau, G W Canonica, C Jasmin, B Azzarone

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
9.7field-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

121 citing papers in PubMed, 356 citations in OpenAlex.

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  12. Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023
    Article
  13. Review
  14. Article
  15. Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.The Journal of allergy and clinical immunology · 2022
    Review
  16. Article
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  18. Article
  19. Translational targeting of inflammation and fibrosis in frozen shoulder: Molecular dissection of the T cell/IL-17A axis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Review

61 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

6 authors at 3 institutions in 2 countries.

C DoucetU268 INSERM Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
D Brouty-Boyé
C Pottin-Clémenceau
G W Canonica
C Jasmin
B Azzarone
Hôpital Paul-Brousse · FRIstituto Giannina Gaslini · ITUniversity of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway hyperresponsiveness leading to subepithelial fibrosis is mediated by inflammatory cells activated by T helper (Th) 2-derived cytokines such as IL-4 and IL-5. By analyzing the phenotype and response of human lung fibroblasts derived from either fetal (ICIG7) or adult (CCL202) tissue as well as from a Th2-type stromal reaction (FPA) to IL-4 and IL-13, we provide evidence that human lung fibroblasts may behave as inflammatory cells upon activation by IL-4 and IL-13. We show that the three types of fibroblasts constitute different populations that display a distinct pattern in cell surface molecule expression and proinflammatory cytokine and chemokine release. All fibroblasts express functional but different IL-4/IL-13 receptors. Thus, while IL-4 receptor (R) alpha and IL-13Ralpha1 chains are present in all the cells, CCL202 and FPA fibroblasts coexpress the IL-13Ralpha2 and the IL-2Rgamma chain, respectively, suggesting the existence of a heterotrimeric receptor (IL-4Ralpha/IL-13Ralpha/IL-2Rgamma) able to bind IL-4 and IL-13. Stimulation with IL-4 or IL-13 triggers in the fibroblasts a differential signal transduction and upregulation in the expression of beta1 integrin and vascular cell adhesion molecule 1 and in the production of IL-6 and monocyte chemoattractant protein 1, two inflammatory cytokines important in the pathogenesis of allergic inflammation. Our results suggest that when activated by IL-4 and IL-13, different subsets of lung fibroblasts may act as effector cells not only in the pathogenesis of asthma but also in lung remodeling processes. They may also differentially contribute to trigger and maintain the recruitment, homing, and activation of inflammatory cells.

Indexed as

Antigens, SurfaceAsthmaCell Adhesion MoleculesCell LineChemokinesCross-Linking ReagentsCytokinesFlow CytometryGene Expression RegulationHumansHypersensitivityInflammationInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4LungAntigens, SurfaceCell Adhesion MoleculesChemokinesCross-Linking ReagentsCytokinesIL13RA1 protein, humanInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4PhosphotyrosineReceptors, InterleukinReceptors, Interleukin-13Receptors, Interleukin-4RNA, Messenger

Identifiers

PMID9593769
PMCPMC508801
OpenAlexW2045873742

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.