Evidence map›Paper›PMID 28842670›Full record

ArticleScientific reports2017

The cellular and molecular determinants of emphysematous destruction in COPD.

Masaru Suzuki, Marc A Sze, Joshua D Campbell, John F Brothers, Marc E Lenburg, John E McDonough, W Mark Elliott, Joel D Cooper, Avrum Spira, James C Hogg

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

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  19. The Role of Group 3 Innate Lymphoid Cells in Lung Infection and Immunity.Frontiers in cellular and infection microbiology · 2021
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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

10 authors at 3 institutions in 3 countries.

Masaru SuzukiCentre for Heart Lung Innovation, St. Paul's Hospital, Departments of Medicine, and Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.ORCID 0000-0002-2124-6793
Marc A SzeCentre for Heart Lung Innovation, St. Paul's Hospital, Departments of Medicine, and Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.ORCID 0000-0002-3532-9653
Joshua D CampbellDivision of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
John F BrothersDivision of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Marc E LenburgDivision of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
John E McDonoughCentre for Heart Lung Innovation, St. Paul's Hospital, Departments of Medicine, and Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.
W Mark ElliottCentre for Heart Lung Innovation, St. Paul's Hospital, Departments of Medicine, and Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.
Joel D CooperDivision of Thoracic Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA, USA.
Avrum SpiraDivision of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
James C HoggCentre for Heart Lung Innovation, St. Paul's Hospital, Departments of Medicine, and Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada. Jim.Hogg@hli.ubc.ca.
University of British Columbia · CABoston University · USHospital of the University of Pennsylvania · US

Funding

BIOLOGY OF THE LUNG--MULTIDISCIPLINARY PROGRAMT32HL007035 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Darrell N. Kotton, JOSEPH P MIZGERD · 1985 to 2026
$24.3M
CIHRNHLBI NIH HHS T32 HL007035
6 · The paper itself

Abstract

The introduction of microCT has made it possible to show that the terminal bronchioles are narrowed and destroyed before the onset of emphysematous destruction in COPD. This report extends those observations to the cellular and molecular level in the centrilobular phenotype of emphysematous destruction in lungs donated by persons with very severe COPD (n = 4) treated by lung transplantation with unused donor lungs (n = 4) serving as controls. These lung specimens provided companion samples to those previously examined by microCT (n = 61) that we examined using quantitative histology (n = 61) and gene expression profiling (n = 48). The histological analysis showed that remodeling and destruction of the bronchiolar and alveolar tissue is associated with macrophage, CD4, CD8, and B cell infiltration with increased formation of tertiary lymphoid organs. Moreover, gene set enrichment analysis showed that genes known to be expressed by natural killer (NK), lymphoid tissue inducer (LTi), and innate lymphoid cell 1 (ILC1) cells, but not ILC2 or ILC3 cells, were enriched in the expression profiles associated with CD4, CD8, and B cell infiltration. Based on these findings, we postulate that the centrilobular phenotype of emphysematous destruction COPD is driven by a Th1 response activated by infiltrating ILC1, NK, and LTi cells.

Indexed as

BiomarkersBiopsyFemaleGene Expression ProfilingHumansImmune SystemMaleMiddle AgedPulmonary Disease, Chronic ObstructivePulmonary EmphysemaRespiratory Function TestsRisk FactorsX-Ray MicrotomographyBiomarkers

Identifiers

PMID28842670
PMCPMC5573394
OpenAlexW2746932197

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.