Evidence map›Paper›PMID 28468623›Full record

ArticleRespiratory research2017

Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium.

Lynne A Murray, Rebecca Dunmore, Ana Camelo, Carla A Da Silva, Malin J Gustavsson, David M Habiel, Tillie L Hackett, Cory M Hogaboam, Matthew A Sleeman, Darryl A Knight

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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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 5 institutions in 5 countries.

Lynne A MurrayRespiratory, Inflammation and Autoimmunity, MedImmune Ltd, Granta Park, Cambridge, CB21 6GH, United Kingdom. murrayl@medimmune.com.
Rebecca DunmoreRespiratory, Inflammation and Autoimmunity, MedImmune Ltd, Granta Park, Cambridge, CB21 6GH, United Kingdom.
Ana CameloRespiratory, Inflammation and Autoimmunity, MedImmune Ltd, Granta Park, Cambridge, CB21 6GH, United Kingdom.
Carla A Da SilvaRespiratory, Inflammation and Autoimmunity innovative Medicines Unit, AstraZeneca R&D, Mölndal, Sweden.
Malin J GustavssonRespiratory, Inflammation and Autoimmunity innovative Medicines Unit, AstraZeneca R&D, Mölndal, Sweden.
David M HabielDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Tillie L HackettDepartment of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, Canada.
Cory M HogaboamDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Matthew A SleemanRespiratory, Inflammation and Autoimmunity, MedImmune Ltd, Granta Park, Cambridge, CB21 6GH, United Kingdom.
Darryl A KnightDepartment of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, Canada.
Aimmune Therapeutics (United Kingdom) · GBAstraZeneca (Sweden) · SECedars-Sinai Medical Center · USUniversity of British Columbia · CAUniversity of Newcastle Australia · AU

Funding

Innate DNA sensing in rapidly progressing IPFR01HL123899 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI HOGABOAM, CORY M · 2015 to 2018
$2.0M
NHLBI NIH HHS R01 HL123899
6 · The paper itself

Abstract

backgroundSmoking and aberrant epithelial responses are risk factors for lung cancer as well as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. In these conditions, disease progression is associated with epithelial damage and fragility, airway remodelling and sub-epithelial fibrosis. The aim of this study was to assess the acute effects of cigarette smoke on epithelial cell phenotype and pro-fibrotic responses in vitro and in vivo.

resultsApoptosis was significantly greater in unstimulated cells from COPD patients compared to control, but proliferation and CXCL8 release were not different. Cigarette smoke dose-dependently induced apoptosis, proliferation and CXCL8 release with normal epithelial cells being more responsive than COPD patient derived cells. Cigarette smoke did not induce epithelial-mesenchymal transition. In vivo, cigarette smoke exposure promoted epithelial apoptosis and proliferation. Moreover, mimicking a virus-induced exacerbation by exposing to mice to poly I:C, exaggerated the inflammatory responses, whereas expression of remodelling genes was similar in both.

conclusionsCollectively, these data indicate that cigarette smoke promotes epithelial cell activation and hyperplasia, but a secondary stimulus is required for the remodelling phenotype associated with COPD.

Indexed as

AnimalsApoptosisEpithelial-Mesenchymal TransitionHumansMiceMice, Inbred C57BLPulmonary Disease, Chronic ObstructivePulmonary FibrosisRespiratory MucosaSmokeTobacco ProductsSmokeApoptosisPoly I:CRemodellingTGFβ1

Identifiers

PMID28468623
PMCPMC5415733
OpenAlexW2610371466

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.