Evidence map›Paper›PMID 27297409›Full record

Trial reportBMC pulmonary medicine2016

Eosinophils enhance WNT-5a and TGF-β1 genes expression in airway smooth muscle cells and promote their proliferation by increased extracellular matrix proteins production in asthma.

Andrius Januskevicius, Simona Vaitkiene, Reinoud Gosens, Ieva Janulaityte, Deimante Hoppenot, Raimundas Sakalauskas, Kestutis Malakauskas

2 registry-linked trialsOpen access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in BMC pulmonary medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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.

NCT02648074 nacompletednot on this map

Eosinophil Induced Airway Smooth Muscle Remodelling in Asthma

TypeinterventionalSponsorLithuanian University of Health SciencesRan2014 to 2017Enrolled20ConditionsAllergic Asthma, Airway RemodellingArmsBronchial challenge with allergen, Co-culture formation
NCT03388359 naunknown statusnot on this mapstarted 2017, after this paper: background citation

Role of Extracellular Matrix in the Development of Airway Remodeling in Asthma

TypeinterventionalSponsorLithuanian University of Health SciencesRan2017 to 2020Enrolled60ConditionsAllergic Asthma, Airway Remodelling, Extracellular Matrix AlterationArmsBronchial challenge with allergen, Co-culture formation, Inhibition of Wnt and Smad signaling pathways, Extracellular matrix turnover and deposition assessment, Dermatophagoides pteronyssinus allergen
3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Distinct miRNA expression patterns in circulating eosinophil subtypes and their subtype-derived exosomes in allergic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Wnt signaling - using the bloodstream to send a message.Cellular and molecular life sciences : CMLS · 2025
    Review
  5. Review
  6. Article
  7. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  8. Review
  9. The molecular mechanisms of remodeling in asthma, COPD and IPF with a special emphasis on the complex role of Wnt5A.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  10. Article
  11. Noncanonical Wnt Signaling Promotes Myofibroblast Differentiation in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021
    Article
  12. Review
  13. αJournal of personalized medicine · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. WNT Signalling in Lung Physiology and Pathology.Handbook of experimental pharmacology · 2021
    Article
  18. Article
  19. Article
  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

7 authors at 2 institutions in 2 countries.

Andrius JanuskeviciusLaboratory of Pulmonology, Department of Pulmonology and Immunology, Lithuanian University of Health Sciences, Eiveniu str. 2, Kaunas, LT-50009, Lithuania. Andriusjanuskevicius.11@gmail.com.ORCID http://orcid.org/0000-0001-9016-9149
Simona VaitkieneLaboratory of Pulmonology, Department of Pulmonology and Immunology, Lithuanian University of Health Sciences, Eiveniu str. 2, Kaunas, LT-50009, Lithuania.
Reinoud GosensDepartment of Molecular Pharmacology, University of Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands.
Ieva JanulaityteLaboratory of Pulmonology, Department of Pulmonology and Immunology, Lithuanian University of Health Sciences, Eiveniu str. 2, Kaunas, LT-50009, Lithuania.
Deimante HoppenotDepartment of Pulmonology and Immunology, Lithuanian University of Health Sciences, Eiveniu str. 2, Kaunas, LT-50009, Lithuania.
Raimundas SakalauskasDepartment of Pulmonology and Immunology, Lithuanian University of Health Sciences, Eiveniu str. 2, Kaunas, LT-50009, Lithuania.
Kestutis MalakauskasLaboratory of Pulmonology, Department of Pulmonology and Immunology, Lithuanian University of Health Sciences, Eiveniu str. 2, Kaunas, LT-50009, Lithuania.
Lithuanian University of Health Sciences · LTUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have suggested that eosinophils may have a direct effect on airway smooth muscle cells (ASMC), causing their proliferation in patients with asthma, but the precise mechanism of the interaction between these cells remains unknown. We propose that changes in Wnt signaling activity and extracellular matrix (ECM) production may help explain these findings. Therefore, the aim of this study was to investigate the effect of eosinophils from asthmatic and non-asthmatic subjects on Wnt-5a, transforming growth factor β1 (TGF-β1), and ECM protein (fibronectin and collagen) gene expression and ASMC proliferation.

methodsA total of 18 subjects were involved in the study: 8 steroid-free asthma patients and 10 healthy subjects. Peripheral blood eosinophils were isolated using centrifugation and magnetic separation. An individual co-culture of eosinophils with human ASMC was prepared for each study subject. Adhesion of eosinophils to ASMC (evaluated by assaying eosinophil peroxidase activity) was determined following various incubation periods (30, 45, 60, 120, and 240 min). The expression of Wnt-5a, TGF-β1, and ECM protein genes in ASMC was measured using quantitative real-time polymerase chain reaction (PCR) after 24 h of co-culture. Proliferation of ASMC was measured using the Alamar blue method after 48 h and 72 h of co-culture with eosinophils.

resultsEosinophils from asthmatic subjects demonstrated increased adhesion to ASMC compared with eosinophils from healthy subjects (p < 0.05) in vitro. The expression of Wnt-5a, TGF-β1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-β1 and fibronectin gene expression. ASMC proliferation was augmented after co-culture with eosinophils from asthma patients compared with co-culture with eosinophils from healthy subjects (p < 0.05).

conclusionsEosinophils enhance Wnt-5a, TGF-β1, fibronectin, and collagen gene expression in ASMC and promote proliferation of these cells in asthma.

trial registrationClinicalTrials.gov Identifier: NCT02648074 .

Indexed as

AdultAsthmaCase-Control StudiesCell ProliferationCells, CulturedCoculture TechniquesCollagenEosinophilsExtracellular Matrix ProteinsFemaleFibronectinsHumansMaleMyocytes, Smooth MuscleSignal TransductionTransforming Growth Factor beta1CollagenExtracellular Matrix ProteinsFibronectinsFN1 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1Wnt-5a ProteinWNT5A protein, humanAdhesionAirway smooth muscle cellsAsthmaCollagenEosinophilsFibronectinProliferationTGF-β1WNT-5a

Identifiers

PMID27297409
PMCPMC4906992
OpenAlexW2434461128

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LicenceCC BY
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Registered trials

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.