Evidence map›Paper›PMID 33602992›Full record

ArticleScientific reports2021

The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD.

Miranda P Ween, Jake B White, Hai B Tran, Violet Mukaro, Charles Jones, Matthew Macowan, Gregory Hodge, Paul J Trim, Marten F Snel, Sandra J Hodge

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. 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
3.2field-weighted citation impact, top 7% 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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  11. E-Cigarette Vapour Increases ACE2 and TMPRSS2 Expression in a Flavour- and Nicotine-Dependent Manner.International journal of environmental research and public health · 2022
    Article
  12. Article
  13. Review
  14. Revisiting the role of pulmonary surfactant in chronic inflammatory lung diseases and environmental exposure.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
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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 1 country.

Miranda P WeenDepartment of Thoracic Medicine, Royal Adelaide Hospital, Adelaide, Australia. miranda.ween@adelaide.edu.au.
Jake B WhiteSchool of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Hai B TranDepartment of Thoracic Medicine, Royal Adelaide Hospital, Adelaide, Australia.
Violet MukaroDepartment of Thoracic Medicine, Royal Adelaide Hospital, Adelaide, Australia.
Charles JonesSchool of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Matthew MacowanDepartment of Thoracic Medicine, Royal Adelaide Hospital, Adelaide, Australia.
Gregory HodgeDepartment of Thoracic Medicine, Royal Adelaide Hospital, Adelaide, Australia.
Paul J TrimSchool of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Marten F SnelSchool of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Sandra J HodgeSchool of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Royal Adelaide Hospital · AUUniversity of Adelaide · AUSouth Australian Health and Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In chronic obstructive pulmonary disease (COPD) apoptotic bronchial epithelial cells are increased, and their phagocytosis by alveolar macrophages (AM) is decreased alongside bacterial phagocytosis. Epithelial cellular lipids, including those exposed on uncleared apoptotic bodies, can become oxidized, and may be recognized and presented as non-self by antigen presenting cells. CD1b is a lipid-presenting protein, previously only described in dendritic cells. We investigated whether CD1b is upregulated in COPD AM, and whether lipid oxidation products are found in the airways of cigarette smoke (CS) exposed mice. We also characterise CD1b for the first time in a range of macrophages and assess CD1b expression and phagocytic function in response to oxidised lipid. Bronchoalveolar lavage and exhaled breath condensate were collected from never-smoker, current-smoker, and COPD patients and AM CD1b expression and airway 8-isoprostane levels assessed. Malondialdehyde was measured in CS-exposed mouse airways by confocal/immunofluorescence. Oxidation of lipids produced from CS-exposed 16HBE14o- (HBE) bronchial epithelial cells was assessed by spectrophotometry and changes in lipid classes assessed by mass spectrometry. 16HBE cell toxicity was measured by flow cytometry as was phagocytosis, CD1b expression, HLA class I/II, and mannose receptor (MR) in monocyte derived macrophages (MDM). AM CD1b was significantly increased in COPD smokers (4.5 fold), COPD ex-smokers (4.3 fold), and smokers (3.9 fold), and AM CD1b significantly correlated with disease severity (FEV

Indexed as

Lipid MetabolismAdultAgedAged, 80 and overAnimalsAntigens, CD1Bronchoalveolar Lavage FluidFemaleFlow CytometryForced Expiratory VolumeGas Chromatography-Mass SpectrometryHumansMacrophages, AlveolarMaleMalondialdehydeMass SpectrometryAntigens, CD1CD1b antigenMalondialdehydeTobacco Smoke Pollution

Identifiers

PMID33602992
PMCPMC7892841
OpenAlexW3132488414

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.