Evidence map›Paper›PMID 34867934›Full record

ArticleFrontiers in immunology2021

Collagen 1a1 Expression by Airway Macrophages Increases In Fibrotic ILDs and Is Associated With FVC Decline and Increased Mortality.

Eliza Tsitoura, Athina Trachalaki, Eirini Vasarmidi, Semeli Mastrodemou, George A Margaritopoulos, Maria Kokosi, Dionysios Fanidis, Apostolos Galaris, Vassilis Aidinis, Elizabeth Renzoni and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 31 citations in OpenAlex.

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  15. Effect of CTMP1 gene on pulmonary fibrosis.Toxicological research · 2025
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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

13 authors at 5 institutions in 2 countries.

Eliza TsitouraLaboratory of Molecular and Cellular Pneumonology, Department of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
Athina TrachalakiLaboratory of Molecular and Cellular Pneumonology, Department of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
Eirini VasarmidiLaboratory of Molecular and Cellular Pneumonology, Department of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
Semeli MastrodemouLaboratory of Molecular and Cellular Pneumonology, Department of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
George A MargaritopoulosInterstitial Lung Disease Unit, Royal Brompton and Harefield Hospital National Health Service (NHS) Foundation Trust, Imperial College, London, United Kingdom.
Maria KokosiInterstitial Lung Disease Unit, Royal Brompton and Harefield Hospital National Health Service (NHS) Foundation Trust, Imperial College, London, United Kingdom.
Dionysios FanidisDivision of Immunology, Alexander Fleming Biomedical Sciences Research Centre, Athens, Greece.
Apostolos GalarisDivision of Immunology, Alexander Fleming Biomedical Sciences Research Centre, Athens, Greece.
Vassilis AidinisDivision of Immunology, Alexander Fleming Biomedical Sciences Research Centre, Athens, Greece.
Elizabeth RenzoniInterstitial Lung Disease Unit, Royal Brompton and Harefield Hospital National Health Service (NHS) Foundation Trust, Imperial College, London, United Kingdom.
Nikos TzanakisLaboratory of Molecular and Cellular Pneumonology, Department of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
Athol U WellsInterstitial Lung Disease Unit, Royal Brompton and Harefield Hospital National Health Service (NHS) Foundation Trust, Imperial College, London, United Kingdom.
Katerina M AntoniouLaboratory of Molecular and Cellular Pneumonology, Department of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
University of Crete · GRAlexander Fleming Biomedical Sciences Research Center · GRRoyal Brompton & Harefield NHS Foundation Trust · GBHarefield Hospital · GBImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Within the Interstitial Lung Diseases (ILD), patients with idiopathic pulmonary fibrosis (IPF) and a subset of those with non-IPF fibrotic ILD have a distinct clinical phenotype of progression despite management. This group of patients has been collectively termed the progressive fibrotic phenotype (PFP). Their early recognition may facilitate access to antifibrotic therapies to prevent or slow progression. Macrophages/monocytes within the lung orchestrate the progression and maintenance of fibrosis. A novel role for monocyte-derived macrophages during tissue damage and wound healing is the expression of collagens. We examined Collagen 1a1 expression in airway macrophages from ILD patients at diagnosis. COL1A1 mRNA levels from BAL cells were elevated in IPF and Non-IPF patients. The presence of a UIP pattern and a subsequent progressive phenotype were significantly associated with the higher BAL COL1A1 levels. In Non-IPF patients, higher COL1A1 levels were associated with a more than twofold increase in mortality. The intracellular localisation of COL1A1 in airway macrophages was demonstrated by confocal microscopy in CD45 and CD163 co-staining assays. Additionally, airway macrophages co-expressed COL1A1 with the profibrotic SPP1 gene product osteopontin. The levels of SPP1 mRNA and OPN in the BAL were significantly higher in IPF and Non-IPF patients relative to healthy. Our results suggest that profibrotic airway macrophages are increased in the BAL of patients with IPF and other ILDs and co-express COL1A1 and OPN. Importantly, COL1A1 expression by pro-fibrotic airway macrophages could be a marker of disease progression and poor survival in ILDs.

Indexed as

AdultAgedAnimalsBronchoalveolar Lavage FluidCase-Control StudiesCollagen Type I, alpha 1 ChainDisease Models, AnimalDisease ProgressionFemaleFibrosisHumansIdiopathic Pulmonary FibrosisLungLung Diseases, InterstitialMacrophages, AlveolarMaleCOL1A1 protein, humanCol1a1 protein, mouseCollagen Type I, alpha 1 ChainOsteopontinRNA, MessengerSPP1 protein, humanairway macrophagescollagen 1A1IPFNSIPosteopontinPF-ILDRA-ILDSPP1

Identifiers

PMID34867934
PMCPMC8635798
OpenAlexW3213485301

What OpenQuestion holds

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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.