ArticleERJ open research2025
Alveolar macrophage carbon is associated with COPD severity.
Article in ERJ open research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed.
- From metabolic alterations to chronic inflammation: mechanisms and immunoregulation of metabolic reprogramming in COPD.Frontiers in immunology · 2025Review
- ERS International Congress 2023: highlights from the Airway Diseases Assembly.ERJ open research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: COPD is driven by the inhalation of noxious particles. A significant component of particulate matter is carbon, which is taken up by alveolar macrophages. We compared alveolar macrophage carbon levels in COPD patients to smokers and assessed the relationship of carbon load with macrophage size and phenotype. Methods: Lung tissue from COPD patients (n=28) and smokers (n=15) was stained for alveolar macrophages. The area of carbon deposits within macrophages and macrophage size were measured. The effect of carbon exposure on macrophage size, phenotype marker expression (real-time PCR) and pro-inflammatory cytokine production (tumour necrosis factor-α (TNF-α) and CXCL8 by ELISA) was assessed Results: Carbon area (µm Conclusions: Alveolar macrophage carbon was increased in COPD patients compared to smokers and negatively correlated with lung function. Carbon skews macrophages to a phenotype of increased size and differential expression of macrophage phenotype genes. Alveolar macrophage carbon exposure may be a significant driver of macrophage dysfunction in COPD.
Identifiers
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Registered trials
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.