Journal
TUBERCULOSIS AND RESPIRATORY DISEASES
Volume 80, Issue 1, Pages 60-68Publisher
TAEHAN KYORHAEK HYOPHOE-KOREAN ACAD TUBERCULOSIS & RESPIRATORY DISEASES
DOI: 10.4046/trd.2017.80.1.60
Keywords
Mometasone Fuorate; Budesonide; Mucins; MUC2 Protein, Human; MUC5AC Protein, Human; Tumor Necrosis Factor-Alpha; Epithelial Cells
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Funding
- Thammasat University, Thailand
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Background: Mucus hypersecretion from airway epithelium is a characteristic feature of airway inflammatory diseases. Tumor necrosis factor alpha (TNF-alpha) regulates mucin synthesis. Glucocorticoids including mometasone fuorate (MF) have been used to attenuate airway inflammation. However, effects of MF on mucin production have not been reported. Methods: Effects of MF and budesonide (BUD) on the phorbol-12-myristate-13-acetate (PMA)-induction of mucin and TNF-alpha in human airway epithelial cells (NCI-H292) were investigated in the present study. Confluent NCI-H292 cells were pretreated with PMA (200 nM) for 2 hours. Subsequently, the cells were stimulated with MF (1-500 ng/mL) or BUD (21.5 ng/mL) for 8 hours. Dexamethasone (1 mu g/mL) was used as the positive control. Real-time polymerase chain reaction was used to determine MUC2 and MUC5AC mRNA levels. The level of total mucin, MUC2, MUC5AC, and TNF-alpha in culture supernatants were measured using enzyme-linked immunosorbent assay. Results: MF and BUD significantly suppressed MUC2 and MUC5AC gene expression in PMA-stimulated NCI-H292 cells. The inhibitory effects of the two steroid drugs were also observed in the production of total mucin, MUC2 and MUC5AC proteins, and TNF-alpha. Conclusion: Our findings demonstrated that MF and BUD attenuated mucin and TNF-alpha production in PMA-induced human airway epithelial cells.
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