MUC5B regulates the airway inflammation induced by atmospheric PM_2.5 in rats and A549 cells

Atmospheric PM_2.5 can induce airway inflammation and mucin secretion. MUC5B is required for airway defense. However, the research on the role of MUC5B in airway inflammation induced by atmospheric PM_2.5 remains limited. This study was designed to explore the role of MUC5B in airway inflammation induced by atmospheric PM_2.5. In vivo, Wistar rats were exposed to 0, 1.5, 7.5, 37.5 mg/ kg PM_2.5 saline suspension via intratracheal instillation. HE staining and AB-PAS staining were used to observe the airway inflammation and goblet cell hyperplasia. In vitro, normal A549 cells and MUC5B-knockdown A549 cells were exposed to 0, 100, 200 and 400 μg/mL PM_2.5 for 6 h, 12 h, 24 h and 48 h. ELISA was used to measure the levels of TNF-α and IL-1β in serum and bronchoalveolar lavage fluid of rats and in cell culture. Real time-PCR and ELISA were used to quantify the mRNA and protein levels of MUC5B in trachea and lung of rats and in A549 cells. PM_2.5 could cause the infiltration of inflammatory cells and increase the mucus secretions and goblet cell metaplasia. MUC5B is related to rats' airway inflammation induced by PM_2.5. A549 cells exposed to PM_2.5 in higher concentration and longer time, the protein level of MUC5B was significantly increased, while the levels of IL-1β, TNF-α and MUC5B mRNA were significantly decreased. Compared with normal A549 cells, the levels of IL-1β and TNF-α were significantly higher in Muc5b-knockdown cells. Atmospheric PM_2.5 can induce airway inflammation and mucin secretion. MUC5B played a critical role in controlling the inflammatory response induced by PM_2.5.