Misiukiewicz-Stępień Paulina, Zajusz-Zubek Elwira, Górska Katarzyna, Krenke Rafał, Paplińska-Goryca Magdalena
Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, Warsaw, 02-097, Poland.
Faculty of Energy and Environmental Engineering, Department of Air Protection, Silesian University of Technology, Gliwice, Poland.
Respir Res. 2025 Jan 8;26(1):8. doi: 10.1186/s12931-025-03097-w.
Pathobiology of asthma and chronic obstructive pulmonary disease (COPD) is associated with changes among respiratory epithelium structure and function. Increased levels of PM from urban particulate matter (UPM) are correlated with enlarged rate of asthma and COPD morbidity as well as acute disease exacerbation. It has been suggested that pre-existing pulmonary obstructive diseases predispose epithelium for different biological response than in healthy airways. The aim of this study was to assess the impact of PM on the biological response of healthy as well as asthma and COPD respiratory epithelium using 3D/spheroid culture model.
The spheroids from 5 healthy controls, 8 asthma patients, and 8 COPD patients were exposed to 100 µg/ml of PM for 24 h.
The common pattern for healthy asthma and COPD epithelium inflammatory response to PM stimulation include the increase in IL-1β, IL-6, IL-8 mRNA expression, and secretion of IL-6. Asthmatic spheroids produced higher amount of TNF-α and IL-8, whereas COPD spheroids expressed increased mRNA level of MUC5AC and decreased level of MMP7. PM treatment induced changes in AHR and TLR4 expression on secretory epithelium in COPD.
The response of airway epithelium to air pollution is different in healthy people than in obstructive lung disease patients. The impairment of airway epithelium in asthma and COPD changes their response to toxic environmental stimuli. This physiological dysfunction might be associated with diseases exacerbation of obstructive lung diseases.
哮喘和慢性阻塞性肺疾病（COPD）的病理生物学与呼吸道上皮结构和功能的变化有关。城市颗粒物（UPM）中PM水平的升高与哮喘和COPD发病率的增加以及急性疾病加重相关。有人提出，与健康气道相比，预先存在的肺阻塞性疾病使上皮细胞产生不同的生物学反应。本研究的目的是使用3D/球体培养模型评估PM对健康以及哮喘和COPD呼吸道上皮细胞生物学反应的影响。
将来自5名健康对照者、8名哮喘患者和8名COPD患者的球体暴露于100µg/ml的PM中24小时。
健康、哮喘和COPD上皮细胞对PM刺激的炎症反应的共同模式包括IL-1β、IL-6、IL-8 mRNA表达增加以及IL-6分泌增加。哮喘球体产生的TNF-α和IL-8量更高，而COPD球体中MUC5AC的mRNA水平升高，MMP7水平降低。PM处理导致COPD分泌上皮细胞的气道高反应性（AHR）和TLR4表达发生变化。
健康人与阻塞性肺疾病患者的气道上皮对空气污染的反应不同。哮喘和COPD中气道上皮的损伤改变了它们对有毒环境刺激的反应。这种生理功能障碍可能与阻塞性肺疾病的疾病加重有关。
