Increased airway T lymphocyte microparticles in chronic obstructive pulmonary disease induces airway epithelial injury.

In our previous study, T lymphocyte microparticles (TLMPs) originated from CEM T lymphoblast-like cell line induced enhanced production of inflammation-associated cytokines and apoptosis in human bronchial epithelial cells (HBEs). To measure TLMP subpopulations in bronchoalveolar lavage fluids (BALF) from patients with chronic obstructive pulmonary disease (COPD), and to explore the effects of MPs derived from different T cell subpopulations on airway epithelium, this study was conducted. A hospital-based case-control study including 47 COPD patients and 28 healthy volunteers was performed. The cellular origins of MPs from airway in COPD and controls were evaluated using flow cytometry. CD4+ or CD8+ TLMPs were isolated by MACS to investigate their effects on HBEs in vitro. The numbers of MPs derived from T lymphocytes in BALF as well as these subpopulations (CD4+ and CD8+ T lymphocytes) were significantly upregulated in COPD patients compared with healthy volunteers. However, there was no significant difference between stable COPD and patients with acute exacerbation. Additionally, significant correlation between CD4+ and CD8+ TLMPs was observed, however neither type nor total level of TLMPs was correlated with any base parameter. Furthermore, isolated CD4+ and CD8+ TLMPs reduced cell viability and induced significant production of inflammatory cytokines including interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, MCP-2, matrix metallopeptidase (MMP)-9 and tumor necrosis factor-alpha (TNF-α) in HBEs, while the levels of anti-inflammatory cytokine IL-10 were decreased. TLMPs in the airways, as putative biomarkers, may lead to airway epithelial injury and inflammation and serve essential roles in the pathophysiology of COPD.