Evidence map›Paper›PMID 41550953›Full record

ArticleFrontiers in immunology2025

Bronchial epithelial cell-derived extracellular vesicles drive inflammasome activation and

Georgia Bateman, Hong Guo-Parke, Caitlyn Harvey, Aoife Rodgers, Anna Krasnodembskaya, Dermot Linden, Rabindra Tirouvanziam, Lee A Borthwick, Andrew J Fisher, Judith Coppinger and 2 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Georgia BatemanAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.
Hong Guo-ParkeAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.
Caitlyn HarveyAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.
Aoife RodgersAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.
Anna KrasnodembskayaAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.
Dermot LindenAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.
Rabindra TirouvanziamDepartment of Pediatrics, Emory University School of Medicine, Atlanta, GA, United States.
Lee A BorthwickNewcastle Fibrosis Research Group, Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Andrew J FisherInstitute of Transplantation, Newcastle Upon Tyne Hospitals National Health Service (NHS) Foundation Trust, Newcastle Upon Tyne, United Kingdom.
Judith CoppingerSchool of Pharmacy and Biomolecular Sciences, St. Stephen's Green, Dublin, Ireland.
Joe KidneyDepartment of Respiratory Medicine, Mater Hospital, Belfast, United Kingdom.
Clifford C TaggartAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular vesicles (EVs) are lipid-membrane bound vesicles that can be beneficial or detrimental depending on the content they carry. As epithelial cells are the first line of defense against harmful particles, this work explored the role of bronchial epithelial cell-derived EVs (CepEVs) in the pathogenesis and progression of chronic obstructive pulmonary disease (COPD). RNA sequencing of macrophages stimulated with CepEVs revealed the upregulation of various inflammasome-related genes, alongside significant IL-1b and IL-18 release, which could be attenuated with caspase-1 or NLRP3 inhibition. The proteome of CepEVs was also assessed, which highlighted a significant reduction in antibacterial proteins compared to healthy EVs (HepEVs). When functionally assessed in

Indexed as

BronchiEpithelial CellsExtracellular VesiclesInflammasomesPulmonary Disease, Chronic ObstructiveCytokinesHumansMacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinTHP-1 CellsCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinCOPDextracellular vesiclesmacrophagesNLRP3NTHi

Identifiers

PMID41550953
PMCPMC12807989

What Socratic 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 Socratic graph.