Dynamic changes of immune cells and therapeutic responses in experimental models of COPD - PubMed
3 hours ago
- #COPD
- #inflammation
- #immune cells
- COPD is a heterogeneous respiratory disorder with complex pathogenesis involving chronic inflammation, protease-antiprotease imbalance, oxidative stress, and epigenetic regulation.
- Experimental models (cigarette smoke exposure, air pollution, acute exacerbation models) help study immune cell dynamics in COPD.
- Macrophages contribute to inflammation and tissue destruction via polarization imbalance and metabolic reprogramming.
- Neutrophils worsen lung injury through recruitment, protease release, NET formation, and delayed apoptosis, while also aiding airway remodeling.
- T cells (CD8+, Th1/Th17, tissue-resident memory T cells) sustain chronic inflammation, whereas impaired Treg function hinders resolution.
- Other immune cells (NK cells, eosinophils, fibrocytes) drive inflammatory amplification and fibrotic remodeling.
- Therapeutic strategies vary: glucocorticoids and PDE4 inhibitors help in eosinophil-driven inflammation, while biologics (IL-5, IL-13/IL-4, TSLP, IL-33) show mixed results.
- Precision phenotyping and personalized immunomodulatory strategies are crucial for COPD treatment.
- Understanding immune cell dynamics in COPD models offers insights into inflammation persistence and therapeutic responses.