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.
Keywords: CCSP/CC16; biomarkers; club cell; fibrosis; occupational exposure.