Otelea Marina Ruxandra, Oancea Corina, Reisz Daniela, Vaida Monica Adriana, Maftei Andreea, Popescu Florina Georgeta
Clinical Department 5, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Department of Physical Medicine and Rehabilitation, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Biomedicines. 2023 Dec 28;12(1):78. doi: 10.3390/biomedicines12010078.
Club cells have a distinct role in the epithelial repair and defense mechanisms of the lung. After exposure to environmental pollutants, during chronic exposure, the secretion of club cells secretory protein (CCSP) decreases. Exposure to occupational hazards certainly has a role in a large number of interstitial lung diseases. According to the American Thoracic Society and the European Respiratory Society, around 40% of the all interstitial lung disease is attributed to occupational hazards. Some of them are very well characterized (pneumoconiosis, hypersensitivity pneumonitis), whereas others are consequences of acute exposure (e.g., paraquat) or persistent exposure (e.g., isocyanate). The category of vapors, gases, dusts, and fumes (VGDF) has been proven to produce subclinical modifications. The inflammation and altered repair process resulting from the exposure to occupational respiratory hazards create vicious loops of cooperation between epithelial cells, mesenchymal cells, innate defense mechanisms, and immune cells. The secretions of club cells modulate the communication between macrophages, epithelial cells, and fibroblasts mitigating the inflammation and/or reducing the fibrotic process. In this review, we describe the mechanisms by which club cells contribute to the development of interstitial lung diseases and the potential role for club cells as biomarkers for occupational-related fibrosis.
克拉拉细胞在肺的上皮修复和防御机制中具有独特作用。暴露于环境污染物后，在长期暴露期间，克拉拉细胞分泌蛋白（CCSP）的分泌会减少。接触职业危害因素在大量间质性肺疾病中肯定起到了作用。根据美国胸科学会和欧洲呼吸学会的数据，所有间质性肺疾病中约40%归因于职业危害因素。其中一些疾病特征明确（尘肺、过敏性肺炎），而其他一些则是急性暴露（如百草枯）或持续暴露（如异氰酸酯）的后果。已证实蒸气、气体、粉尘和烟雾（VGDF）类别会产生亚临床改变。接触职业性呼吸道危害因素导致的炎症和修复过程改变，在上皮细胞、间充质细胞、固有防御机制和免疫细胞之间形成了恶性循环。克拉拉细胞的分泌物调节巨噬细胞、上皮细胞和成纤维细胞之间的通讯，减轻炎症和/或减少纤维化过程。在本综述中，我们描述了克拉拉细胞促成间质性肺疾病发展的机制，以及克拉拉细胞作为职业相关纤维化生物标志物的潜在作用。
