Abstract
Long-term inhalation of fine particulate matter (PM(2.5)) has been linked to the onset of various lung diseases. The mucociliary clearance system, acts as the primary host defense mechanism in the airways, with ciliary beat frequency (CBF) being a key parameter for assessing its functionality. The primary aim of this study was to demonstrate the impact of PM(2.5) on CBF and to investigate the potential mechanisms by which PM(2.5) induced changes in CBF through airway axonemes. Airway axonemes were extracted from bovine ciliated epithelium and treated with different concentrations of PM(2.5) in vitro for 10 min and 1 h to simulate short-term and prolonged exposures. Additionally, the pathway was examined using PKA activator (cAMP) and PKA inhibitor (PKI) on ciliary axonemes. The results revealed that PM(2.5) stimulated CBF in airway axonemes via the cAMP-PKA pathway. Low concentrations and short-term exposure to PM(2.5) stimulated CBF elevation, however, high concentration and prolonged exposure to PM(2.5) might damage respiratory cilia, thereby increasing the risk of respiratory diseases.