Xiaodong Zhang, Jie Liu, Jian Sun, Zhan Liu, Hongbo Guo, Weipeng Shao
These findings suggest that PA induces significant but complex, non-progressive modulations in LNs microstructure, cellular proliferation, vascularity, macrophage presence, and lymphatic integrity. This study provides novel insights into the pathophysiological interplay between environmental particulate deposition and regional immune tissue remodeling, warranting further investigation into its potential implications for lymphatic function and immune surveillance in the context of pulmonary pathology.
BACKGROUND: Pleural anthracosis (PA), characterized by the deposition of carbonaceous particles in the subpleural region, is a common pathological finding associated with environmental air pollution, yet its specific impact on regional lymph node (LN) biology remains poorly understood. This study aimed to investigate the structural and functional alterations in subcarinal LNs, correlating these changes with varying degrees of PA.
METHODS: Based on thoracoscopic imaging, PA was categorized into four grades by three associate chief physicians of thoracic surgery, and the PA area ratio was quantified using ImageJ software. The corresponding subcarinal LNs were analyzed via hematoxylin-eosin (HE), Masson's trichrome, Elastica van Gieson (EVG) staining, and immunohistochemistry for Ki67 (proliferation), CD31 (vascular endothelium), CD68 (macrophages), and D2-40 (lymphatic endothelium).
RESULTS: Results demonstrated that increased PA severity was associated with greater accumulation of black particulate matter within the LN capsule and medulla. EVG staining revealed minimal collagen and elastic fiber deposition across most groups, with scant elastic fibers only observed in the highest PA grade (90%). Notably, quantitative analyses of Ki67, CD31, CD68, and D2-40 immunostaining-encompassing positive cell ratio, density, mean optical density, H-score, and Immunoreactive Score (IRS)-all exhibited a consistent non-linear trend, initially increasing and subsequently declining with advancing PA severity.
CONCLUSIONS: These findings suggest that PA induces significant but complex, non-progressive modulations in LNs microstructure, cellular proliferation, vascularity, macrophage presence, and lymphatic integrity. This study provides novel insights into the pathophysiological interplay between environmental particulate deposition and regional immune tissue remodeling, warranting further investigation into its potential implications for lymphatic function and immune surveillance in the context of pulmonary pathology.