Evidence map›Paper›PMID 36414410›Full record

ArticleRespirology (Carlton, Vic.)2023

Smoking induces shifts in cellular composition and transcriptome within the bronchial mucus barrier.

Senani N H Rathnayake, Benedikt Ditz, Jos van Nijnatten, Tayyaba Sadaf, Philip M Hansbro, Corry A Brandsma, Wim Timens, Annemarie van Schadewijk, Peter S Hiemstra, Nick H T Ten Hacken and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Respirology (Carlton, Vic.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Mucins 3A and 3B Are Expressed in the Epithelium of Human Large Airway.International journal of molecular sciences · 2023
    Observational
  7. Article
  8. 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

14 authors at 4 institutions in 2 countries.

Senani N H RathnayakeUniversity of Technology Sydney, Respiratory Bioinformatics and Molecular Biology (RBMB), School of Life Sciences, Sydney, New South Wales, Australia.ORCID 0000-0002-5631-7264
Benedikt DitzDepartment of Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Jos van NijnattenUniversity of Technology Sydney, Respiratory Bioinformatics and Molecular Biology (RBMB), School of Life Sciences, Sydney, New South Wales, Australia.ORCID 0000-0001-5374-0609
Tayyaba SadafUniversity of Technology Sydney, Respiratory Bioinformatics and Molecular Biology (RBMB), School of Life Sciences, Sydney, New South Wales, Australia.
Philip M HansbroCentre for Inflammation, Centenary Institute, and the University of Technology Sydney, Faculty of Science, Sydney, New South Wales, Australia.ORCID 0000-0002-4741-3035
Corry A BrandsmaUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
Wim TimensUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.ORCID 0000-0002-4146-6363
Annemarie van SchadewijkDepartment of Pulmonology, Leiden University Medical Center, Leiden, the Netherlands.
Peter S HiemstraDepartment of Pulmonology, Leiden University Medical Center, Leiden, the Netherlands.ORCID 0000-0002-0238-5982
Nick H T Ten HackenDepartment of Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Brian OliverThe University of Sydney, Respiratory Cellular and Molecular Biology (RCMB), Woolcock Institute of Medical Research, Sydney, New South Wales, Australia.ORCID 0000-0002-7122-9262
Huib A M KerstjensDepartment of Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID 0000-0001-7705-7927
Maarten van den BergeDepartment of Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID 0000-0002-9336-7340
Alen FaizUniversity of Technology Sydney, Respiratory Bioinformatics and Molecular Biology (RBMB), School of Life Sciences, Sydney, New South Wales, Australia.ORCID 0000-0003-1740-3538
University Medical Center Groningen · NLUniversity of Technology Sydney · AULeiden University Medical Center · NLThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveSmoking disturbs the bronchial-mucus-barrier. This study assesses the cellular composition and gene expression shifts of the bronchial-mucus-barrier with smoking to understand the mechanism of mucosal damage by cigarette smoke exposure. We explore whether single-cell-RNA-sequencing (scRNA-seq) based cellular deconvolution (CD) can predict cell-type composition in RNA-seq data.

methodsRNA-seq data of bronchial biopsies from three cohorts were analysed using CD. The cohorts included 56 participants with chronic obstructive pulmonary disease [COPD] (38 smokers; 18 ex-smokers), 77 participants without COPD (40 never-smokers; 37 smokers) and 16 participants who stopped smoking for 1 year (11 COPD and 5 non-COPD-smokers). Differential gene expression was used to investigate gene expression shifts. The CD-derived goblet cell ratios were validated by correlating with staining-derived goblet cell ratios from the COPD cohort. Statistics were done in the R software (false discovery rate p-value < 0.05).

resultsBoth CD methods indicate a shift in bronchial-mucus-barrier cell composition towards goblet cells in COPD and non-COPD-smokers compared to ex- and never-smokers. It shows that the effect was reversible within a year of smoking cessation. A reduction of ciliated and basal cells was observed with current smoking, which resolved following smoking cessation. The expression of mucin and sodium channel (ENaC) genes, but not chloride channel genes, were altered in COPD and current smokers compared to never smokers or ex-smokers. The goblet cell-derived staining scores correlate with CD-derived goblet cell ratios.

conclusionSmoking alters bronchial-mucus-barrier cell composition, transcriptome and increases mucus production. This effect is partly reversible within a year of smoking cessation. CD methodology can predict goblet-cell percentages from RNA-seq.

Indexed as

Pulmonary Disease, Chronic ObstructiveTranscriptomeBiopsyHumansMucusSmokingbronchial mucus barriercellular deconvolutiongene expressiongoblet cellsmoking

Identifiers

PMID36414410
PMCPMC10947540
OpenAlexW4309677664

What OpenQuestion holds

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LicenceCC BY
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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.