Evidence map›Paper›PMID 39934770›Full record

ArticleJournal of inflammation (London, England)2025

Auto-antibodies against carbonyl-modified vimentin in COPD: potential role as a biomarker.

L Heinemann, I Adcock, K F Chung, W Lollinga, M N Hylkema, A Papi, G Caramori, P A Kirkham

Abstract read
In one paragraph

Article in Journal of inflammation (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

8 authors.

L HeinemannNational Heart and Lung Institute, Imperial College London, London, UK.
I AdcockNational Heart and Lung Institute, Imperial College London, London, UK.
K F ChungNational Heart and Lung Institute, Imperial College London, London, UK.
W LollingaDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands.
M N HylkemaDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands.
A PapiRespiratory Medicine, Centro Interdipartimentale per lo Studio delle Malattie Infiammatorie Delle Vie Aeree E Patologie Fumo-Correlate (CEMICEF), University of Ferrara, Ferrara, Italy.
G CaramoriDepartment of Medicine and Surgery, Pulmonology, University of Parma, Parma, Italy.
P A KirkhamNational Heart and Lung Institute, Imperial College London, London, UK. p.kirkham@wlv.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COPD has many hallmarks of autoimmune dysfunction. Driving this autoimmune response are self-antigens, such as highly abundant structural proteins and cellular proteins, which can lead to the production of auto-antibodies. However, controversy surrounds the detection of some of these auto-antibodies as they have often been screened against native, unmodified proteins. Autoantigens arise as a result of a conformational change in the native protein exposing hidden epitopes or by the creation of neo-epitopes through chemical or enzymatic modifications, often caused by oxidative/carbonyl stress. In this study, we screened for auto-antibodies targeting key structural proteins modified by oxidative/carbonyl stress in peripheral blood from stable COPD patients versus control subjects using ELISA. We found an auto-antibody response against unmodified, carbonyl-modified and citrinylated vimentin, with the highest response observed against carbonyl-modified vimentin. Both the IgG and IgM antibody titres against carbonyl-modified were significantly increased in COPD patients compared to healthy non-smokers. Smokers also displayed increased antibody levels against carbonyl-modified vimentin, but only for the IgG isotype. Selectivity analysis indicated that 70% and 63% of COPD patients had higher IgM and IgG titres, respectively, compared to non-smokers. In contrast only 26% and 48% of smokers had higher IgM and IgG titres, respectively, than non-smokers. ROC analysis gave AUC values of 0.78 (p < 0.01) and 0.84 (p < 0.001) for IgM and IgG, respectively, for COPD versus non-smokers, which fell to 0.70 (p < 0.01) and 0.64 (NS), respectively, when asymptomatic smokers were included. No significant increase in antibody titre against carbonyl-modified elastin or collagen was observed in COPD patients or asymptomatic smokers. We conclude that IgM autoantibody responses against carbonyl modified vimentin could serve as a simple blood-based biomarker for COPD, reflecting the disease's pathophysiology, and could help in patient stratification and diagnosis.

Indexed as

BiomarkerCarbonylOxidative stressRespiratory

Identifiers

PMID39934770
PMCPMC11817093

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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.