Evidence map›Paper›PMID 30322354›Full record

ArticleOtolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery2019

Pathologic Fibroblasts in Idiopathic Subglottic Stenosis Amplify Local Inflammatory Signals.

Robert J Morrison, Nicolas-George Katsantonis, Kevin M Motz, Alexander T Hillel, C Gaelyn Garrett, James L Netterville, Christopher T Wootten, Susan M Majka, Timothy S Blackwell, Wonder P Drake and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

43 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  3. The use of centrifugated autologous lipoaspirate in the endoscopic management of idiopathic subglottic stenosis: results from a retrospective non-randomized study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
    Observational
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  17. PD-L1 Acts Independently of PD-1 as a Marker of Pathologic Fibroblasts in Laryngotracheal Stenosis.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2025
    Article
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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

11 authors at 2 institutions in 1 country.

Robert J Morrison1 Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University, Nashville, Tennessee, USA.
Nicolas-George Katsantonis1 Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University, Nashville, Tennessee, USA.
Kevin M Motz3 Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins, Baltimore, Maryland, USA.
Alexander T Hillel3 Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins, Baltimore, Maryland, USA.
C Gaelyn Garrett1 Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University, Nashville, Tennessee, USA.
James L Netterville1 Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University, Nashville, Tennessee, USA.
Christopher T Wootten1 Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University, Nashville, Tennessee, USA.
Susan M Majka4 Department of Pulmonary and Critical Care Medicine, Vanderbilt University, Nashville, Tennessee, USA.
Timothy S Blackwell4 Department of Pulmonary and Critical Care Medicine, Vanderbilt University, Nashville, Tennessee, USA.
Wonder P Drake6 Division of Infectious Disease, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.
Alexander Gelbard1 Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University, Nashville, Tennessee, USA.
Vanderbilt University · USVA Tennessee Valley Healthcare System · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SCHWARTZ, DAVID ALBERT · 2010 to 2020
$21.6M
Role of Lung MSC in EmphysemaR01HL116597 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MAJKA, SUSAN M · 2013 to 2021
$4.4M
Microbial induction of sarcoidosis CD4+ T cell dysfunctionR01HL117074 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL, DRAKE, WONDER P. · 2013 to 2017
$3.8M
Lung MSC regulate angiogenesis and repair during fibrosisR01HL136449 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MAJKA, SUSAN M · 2018 to 2021
$2.5M
Molecular Interrogation of the Host-Pathogen Interface in Idiopathic Subglottic StensosisR01HL146401 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GELBARD, ALEXANDER · 2019 to 2023
$1.9M
Mentoring in Translational Research in Interstitial Lung DiseasesK24HL127301 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Wonder P. Drake · 2016 to 2026
$1.2M
NCI NIH HHS P30 CA068485NHLBI NIH HHS K24 HL127301NHLBI NIH HHS P01 HL092870NHLBI NIH HHS R01 HL116597NHLBI NIH HHS R01 HL117074NHLBI NIH HHS R01 HL136449NHLBI NIH HHS R01 HL146401
6 · The paper itself

Abstract

objectiveTo characterize the phenotype and function of fibroblasts derived from airway scar in idiopathic subglottic stenosis (iSGS) and to explore scar fibroblast response to interleukin 17A (IL-17A). STUDY

designBasic science.

settingLaboratory. SUBJECTS AND

methodsPrimary fibroblast cell lines from iSGS subjects, idiopathic pulmonary fibrosis subjects, and normal control airways were utilized for analysis. Protein, molecular, and flow cytometric techniques were applied in vitro to assess the phenotype and functional response of disease fibroblasts to IL-17A.

resultsMechanistically, IL-17A drives iSGS scar fibroblast proliferation ( P < .01), synergizes with transforming growth factor ß1 to promote extracellular matrix production (collagen and fibronectin; P = .04), and directly stimulates scar fibroblasts to produce chemokines (chemokine ligand 2) and cytokines (IL-6 and granulocyte-macrophage colony-stimulating factor) critical to the recruitment and differentiation of myeloid cells ( P < .01). Glucocorticoids abrogated IL-17A-dependent iSGS scar fibroblast production of granulocyte-macrophage colony-stimulating factor ( P = .02).

conclusionIL-17A directly drives iSGS scar fibroblast proliferation, synergizes with transforming growth factor ß1 to promote extracellular matrix production, and amplifies local inflammatory signaling. Glucocorticoids appear to partially abrogate fibroblast-dependent inflammatory signaling. These results offer mechanistic support for future translational study of clinical reagents for manipulation of the IL-17A pathway in iSGS patients.

Indexed as

Biopsy, NeedleCase-Control StudiesCell ProliferationCells, CulturedCicatrixCytokinesEnzyme-Linked Immunosorbent AssayFemaleFibroblastsFibrosisFlow CytometryHumansImmunohistochemistryInterleukin-17LaryngostenosisMaleCytokinesIL17A protein, humanInterleukin-17fibroblastidiopathic subglottis stenosisIL-17IL-17AiSGSlaryngotracheal stenosistracheal stenosis

Identifiers

PMID30322354
PMCPMC6389372
OpenAlexW2896421189

What OpenQuestion holds

Textmetadata
LicenceTDM
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.