ArticleFrontiers in immunology2023
Mucosal immune alterations at the early onset of tissue destruction in chronic obstructive pulmonary disease.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled 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.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Cell-type specificity of Tim-3 in respiratory diseases: from mechanisms to clinical translation.Frontiers in immunology · 2026Pooled it
- Defective alveolar regeneration in emphysema: identifying dysfunctional cellular crosstalk and novel therapeutic opportunities for tissue repair.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- [Overexpressing NDUFA13 and CRIP1 improves B cell injury and lung Lesions in COPD mouse models].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Joint clinical and molecular subtyping of COPD with variational autoencoders.Nature communications · 2026Article
- PROK2 defines a pathogenic neutrophil subset and serves as a clinical indicator of neutrophilic inflammation in COPD.Respiratory research · 2026Article
- Crosstalk between the microbiome and the mucosal immunoglobulin A system in the lung, in health and disease.Frontiers in cellular and infection microbiology · 2026Review
- Chronic obstructive pulmonary disease reprograms the lung into an immune organ through trained immunity, cell death networks, and immune checkpoint dysregulation.Frontiers in medicine · 2026Article
- Dynamic changes of immune cells and therapeutic responses in experimental models of COPD.Frontiers in immunology · 2026Review
- Computational identification of key genetic drivers in COPD: A first step towards uncovering candidate biomarkers in smokers.Biochemistry and biophysics reports · 2025Article
- An integrated machine learning model of transcriptomic genes in multi-center chronic obstructive pulmonary disease reveals the causal role of TIMP4 in airway epithelial cell.Respiratory research · 2025Article
- Pyroptosis-driven immune dysregulation in COPD: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Biofilm-mediated immune dysregulation in chronic pulmonary diseases: mechanisms and clinical implications.Frontiers in microbiology · 2025Review
- Developmental immune network of airway lymphocytes and innate immune cells in patients with stable COPD.Frontiers in immunology · 2025Article
- The Mediation of Circulating Inflammatory Proteins in the Causal Pathway from Immune Cells to COPD.International journal of chronic obstructive pulmonary disease · 2025Article
- Article
- Review
- Dissecting causal relationships between immune cells, plasma metabolites, and COPD: a mediating Mendelian randomization study.Frontiers in immunology · 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
32 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rationale: COPD is characterized by chronic airway inflammation, small airways changes, with disappearance and obstruction, and also distal/alveolar destruction (emphysema). The chronology by which these three features evolve with altered mucosal immunity remains elusive. This study assessed the mucosal immune defense in human control and end-stage COPD lungs, by detailed microCT and RNA transcriptomic analysis of diversely affected zones. Methods: In 11 control (non-used donors) and 11 COPD (end-stage) explant frozen lungs, 4 cylinders/cores were processed per lung for microCT and tissue transcriptomics. MicroCT was used to quantify tissue percentage and alveolar surface density to classify the COPD cores in mild, moderate and severe alveolar destruction groups, as well as to quantify terminal bronchioles in each group. Transcriptomics of each core assessed fold changes in innate and adaptive cells and pathway enrichment score between control and COPD cores. Immunostainings of immune cells were performed for validation. Results: In mildly affected zones, decreased defensins and increased mucus production were observed, along CD8+ T cell accumulation and activation of the IgA pathway. In more severely affected zones, CD68+ myeloid antigen-presenting cells, CD4+ T cells and B cells, as well as MHCII and IgA pathway genes were upregulated. In contrast, terminal bronchioles were decreased in all COPD cores. Conclusion: Spatial investigation of end-stage COPD lungs show that mucosal defense dysregulation with decreased defensins and increased mucus and IgA responses, start concomitantly with CD8+ T-cell accumulation in mild emphysema zones, where terminal bronchioles are already decreased. In contrast, adaptive Th and B cell activation is observed in areas with more advanced tissue destruction. This study suggests that in COPD innate immune alterations occur early in the tissue destruction process, which affects both the alveoli and the terminal bronchioles, before the onset of an adaptive immune response.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.