Abstract
House dust mite (HDM) is a common allergen of allergic disorders. After exposure to HDM, airway epithelial cells release chemokines to recruit inflammatory cells and cause damage in lung. However, the role of mucin gene in HDM-induced inflammation is not well-known. In this study, we examined how mucin gene regulates HDM-induced inflammation in human airway epithelial cells. We used 0.5ug/ml Der p1 protein, a cystein protease (the major allergen from the dominant mite Dermatophagoides pteronyssinus), to sensitize human pulmonary mucoepidermoid carcinoma H292 cells. The result showed the release of IL-6 was in time-dependent manner raised from 27.08 pg/ml (2-hr exposure) to 463.58 pg/ml (24-hr exposure). The mucin genes, MUC5AC and MUC5B, appear to be the predominant genes expressed and their glycoprotein products are abundant in mucus secretions. The mRNA expression of MUC5AC and MUC5B was evaluated by quantitative real-time PCR. We observed H292 cells started to express MUC5AC and MUC5B after 8-hr Der P1 treatment. The mRNA expression of MUC5AC was hugely increased after HDM exposure. The fold changes compared to non-treated H292 cells were 2.80, 2.38 and 18.29 at 8, 16 and 24 hr, respectively. MUC5B gently expressed in H292 cells different from MUC5AC (The fold changes were 1.72, 0.68 and 1.78 after 8-, 16- and 24-hr exposure). We also found the MUC5AC expression accompanied with excessive IL-6 secretion at the duration of 16-24hr HDM exposure. Excessive mucus contributes to airway obstruction and bacterial infection. The study suggests mite protease mainly up-regulated the expression of MUC5AC resulted in IL-16 secretion. We elucidated the reduction of MUC5AC expression may relieve inflammation.