Evidence map›Paper›PMID 29126429›Full record

ArticleRespiratory research2017

RNA-sequencing analysis of lung primary fibroblast response to eosinophil-degranulation products predicts downstream effects on inflammation, tissue remodeling and lipid metabolism.

Stephane Esnault, Ksenija Bernau, Elizabeth E Torr, Yury A Bochkov, Nizar N Jarjour, Nathan Sandbo

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. A Review of CXCL1 in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2021
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. The combination of machine learning and untargeted metabolomics identifies the lipid metabolism -related gene CH25H as a potential biomarker in asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  7. Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023
    Article
  8. Review
  9. Article
  10. Newborn DNA methylation and asthma acquisition across adolescence and early adulthood.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Increased IL-6 and Potential IL-6 trans-signalling in the airways after an allergen challenge.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Article
  15. Article
  16. Can SARS-CoV-2 Virus Use Multiple Receptors to Enter Host Cells?International journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. Eosinophil cytolysis on Immunoglobulin G is associated with microtubule formation and suppression of rho-associated protein kinase signalling.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020
    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

6 authors at 1 institution in 1 country.

Stephane EsnaultDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, The University of Wisconsin-Madison School of Medicine and Public Health, K4/928 Clinical Science Center MC 9988, 600 Highland Avenue, Madison, WI, 53792, USA. sesnault@medicine.wisc.edu.ORCID http://orcid.org/0000-0001-7238-8671
Ksenija BernauDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, The University of Wisconsin-Madison School of Medicine and Public Health, K4/928 Clinical Science Center MC 9988, 600 Highland Avenue, Madison, WI, 53792, USA.
Elizabeth E TorrDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, The University of Wisconsin-Madison School of Medicine and Public Health, K4/928 Clinical Science Center MC 9988, 600 Highland Avenue, Madison, WI, 53792, USA.
Yury A BochkovDepartment of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI, 53792, USA.
Nizar N JarjourDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, The University of Wisconsin-Madison School of Medicine and Public Health, K4/928 Clinical Science Center MC 9988, 600 Highland Avenue, Madison, WI, 53792, USA.
Nathan SandboDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, The University of Wisconsin-Madison School of Medicine and Public Health, K4/928 Clinical Science Center MC 9988, 600 Highland Avenue, Madison, WI, 53792, USA.
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
Thr Role of Pin1 in AirwayP01HL088594 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 2008 to 2017
$21.0M
Signaling Pathways Regulating Serum Response Factor in Pulmonary FibrosisK08HL093367 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI SANDBO, NATHAN K · 2009 to 2013
$621k
TNS1 in cell-matrix interactions and pulmonary fibrosisR03HL136795 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI SANDBO, NATHAN K · 2017 to 2018
$153k
American Thoracic Society ATS FoundationCoalition for Pulmonary Fibrosis Pulmonary Fibrosis Foundation Research GrantComprehensive Cancer Center, University of Wisconsin P30 CA014520National Center for Advancing Translational Sciences UL1TR000427National Heart, Lung, and Blood Institute NIH HL088594NCATS NIH HHS UL1 TR000427NCI NIH HHS P30 CA014520NHLBI NIH HHS K08 HL093367NHLBI NIH HHS P01 HL088594NHLBI NIH HHS R03 HL136795University of Wisconsin-Madison Development Funding
6 · The paper itself

Abstract

backgroundThe association of eosinophils with inflammation and tissue remodeling is at least partially due to their release of toxic granule proteins and other mediators, including cytokines. Tissue remodeling and consequent functional defects are affected by activity of connective tissue fibroblasts. Exaggerated fibroblast activation, accumulation and change of phenotype may lead to fibrosis and loss of tissue function. So far, little information has been reported on how eosinophils affect inflammation and tissue remodeling via the activation of fibroblasts. We have recently shown that eosinophil activation with IL-3 led to a robust eosinophil degranulation on immunoglobin-G (IgG) coated plates. Thus, in the present study, we analyze the effects of IL-3-activated eosinophil degranulation products on primary human lung fibroblasts (HLF) using whole transcriptome sequencing.

methodsConditioned media was obtained from eosinophils that were pre-activated with IL-3 or IL-5 and subsequently cultured for 6 h on IgG to induce degranulation. This conditioned media was added on human lung fibroblasts (HLF) for 24 h and the cell lysates were then subjected to whole transcriptome sequencing to identify global changes in gene expression. Differentially expressed genes were analyzed using the Ingenuity Pathway Analysis (IPA), and validated by qPCR.

resultsIn HLF, the expression level of 300 genes was changed by conditioned media from IL-3-activated eosinophils compared to control fibroblast cultures. Among these 300 genes, the expression level of 35 genes coding for known proteins was upregulated by IL-3- versus IL-5-pre-activated eosinophils. Of the 35 upregulated genes, IPA identified C3, CH25H, CXCL1, CXCL8, CYP1A1, ICAM1, IL6 and UCN2 as having downstream functions on inflammation, tissue remodeling and lipid synthesis. This analysis combined with previous RNA sequencing analyses of eosinophils suggest IL-1ß, OSM and TNFSF12 as potential upstream regulators of fibroblasts.

conclusionsThis study has identified several novel pro-inflammatory and pro-remodeling mediators produced by fibroblasts in response to activated eosinophils. These findings may have significant implications on the role of eosinophil/fibroblast interactions in eosinophilic disorders.

Indexed as

Cells, CulturedCulture Media, ConditionedEosinophilsFemaleFibroblastsForecastingGene Regulatory NetworksHumansInflammationInflammation MediatorsLipid MetabolismLungSequence Analysis, RNACulture Media, ConditionedInflammation MediatorsDegranulationEosinophilFibroblastIgGIl-3InflammationLipid metabolismLungRNA-sequencingTissue remodeling

Identifiers

PMID29126429
PMCPMC5681771
OpenAlexW2767809721

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.