Single-cell analysis of COPD: Microenvironmental interactions driven by immune-fibrotic imbalance
8 affiliations
- 1School of Nursing, Xinjiang Medical University, Urumqi, Xinjiang, China
- 2Department of Neurology, The Second Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China
- 3School of Basic Medical Science, Xinjiang Medical University, Urumqi, Xinjiang, China
- 4Institute of Medical Sciences of Xinjiang Medical University, Urumqi, Xinjiang, China
- 5School of Public Health, Xinjiang Medical University, Urumqi, Xinjiang, China
- 6Medical Records Management Department, The Affiliated Taian City Central Hospital of Qingdao University, Tai’an, China
- 7Department of Infectious Diseases, Hospital of Traditional Chinese Medicine, Xinjiang Medical University, Urumqi, Xinjiang, China
- 8Department of Pathophysiology, School of Basic Medical Science, Xinjiang Medical University, Urumqi, Xinjiang, China
Abstract
Chronic obstructive pulmonary disease (COPD) is a respiratory disease with a high degree of cellular heterogeneity and molecular complexity, characterized pathologically by persistent airflow limitation and an inflammatory-tissue remodeling cascade involving multiple cell types. Traditional transcriptomics lack the resolution to precisely define cell subpopulation roles in COPD. Single-cell RNA sequencing (scRNA-seq) overcomes this limitation by enabling high-resolution analysis of cell-type-specific mechanisms in COPD. A total of 101,009 cells from three scRNA-seq datasets were integrated to profile COPD-related molecular features and cell interactions at single-cell resolution. Analysis identified four major cell types and 17 distinct cell subtypes. Cell–cell communication analysis revealed a significant reduction in signaling activity of macrophages and fibroblasts, whereas certain immune cells exhibited enhanced signaling, suggesting that immune dysregulation plays a pivotal role in COPD pathogenesis. Further analysis focused on macrophage-dominant myeloid cells and fibroblasts, uncovering their critical roles in inflammation modulation and fibrosis progression. Meanwhile, this study also identified 19 chemicals that may influence COPD progression by modulating cellular gene expression. This study provides an important molecular basis for unraveling the cell-cell interaction network of COPD and elucidating the mechanism of each cell subpopulation in the disease process.
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BibTeX
@article{jiang2026singlecell,
title = {{Single-cell analysis of COPD: Microenvironmental interactions driven by immune-fibrotic imbalance}},
author = {Hong Jiang and Wenxing Wang and Lu Wang and Jiaojian Wu and Jianjiang Luo and Qi Yan and Xueli Gong and Jing Liang},
journal = {PLOS One},
year = {2026},
month = oct,
doi = {10.1371/journal.pone.0361580},
url = {https://doi.org/10.1371/journal.pone.0361580},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Single-cell analysis of COPD: Microenvironmental interactions driven by immune-fibrotic imbalance
AU - Hong Jiang
AU - Wenxing Wang
AU - Lu Wang
AU - Jiaojian Wu
AU - Jianjiang Luo
AU - Qi Yan
AU - Xueli Gong
AU - Jing Liang
PY - 2026
DA - 2026/10/26
JO - PLOS One
DO - 10.1371/journal.pone.0361580
UR - https://doi.org/10.1371/journal.pone.0361580
AB - Chronic obstructive pulmonary disease (COPD) is a respiratory disease with a high degree of cellular heterogeneity and molecular complexity, characterized pathologically by persistent airflow limitation and an inflammatory-tissue remodeling cascade involving multiple cell types. Traditional transcriptomics lack the resolution to precisely define cell subpopulation roles in COPD. Single-cell RNA sequencing (scRNA-seq) overcomes this limitation by enabling high-resolution analysis of cell-type-specific mechanisms in COPD. A total of 101,009 cells from three scRNA-seq datasets were integrated to profile COPD-related molecular features and cell interactions at single-cell resolution. Analysis identified four major cell types and 17 distinct cell subtypes. Cell–cell communication analysis revealed a significant reduction in signaling activity of macrophages and fibroblasts, whereas certain immune cells exhibited enhanced signaling, suggesting that immune dysregulation plays a pivotal role in COPD pathogenesis. Further analysis focused on macrophage-dominant myeloid cells and fibroblasts, uncovering their critical roles in inflammation modulation and fibrosis progression. Meanwhile, this study also identified 19 chemicals that may influence COPD progression by modulating cellular gene expression. This study provides an important molecular basis for unraveling the cell-cell interaction network of COPD and elucidating the mechanism of each cell subpopulation in the disease process.
SN - 1932-6203
ER -