Mometasone Furoate Suppresses PMA-Induced MUC-5AC and MUC-2 Production in Human Airway Epithelial Cells.
	    		
		   		
		   			
		   		
	    	
    	- Author:
	        		
		        		
		        		
			        		Orapan POACHANUKOON
			        		
			        		
			        		
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			        		Sittichai KOONTONGKAEW
			        		
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			        		Paopanga MONTHANAPISUT
			        		
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			        		Napaporn PATTANACHAROENCHAI
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Original Article
 - Keywords: Mometasone Fuorate; Budesonide; Mucins; MUC2 Protein, Human; MUC5AC Protein, Human; Tumor Necrosis Factor-Alpha; Epithelial Cells
 - MeSH: Budesonide; Dexamethasone; Enzyme-Linked Immunosorbent Assay; Epithelial Cells*; Epithelium; Gene Expression; Glucocorticoids; Humans*; Inflammation; Mometasone Furoate*; Mucins; Mucus; Real-Time Polymerase Chain Reaction; RNA, Messenger; Tumor Necrosis Factor-alpha
 - From:Tuberculosis and Respiratory Diseases 2017;80(1):60-68
 - CountryRepublic of Korea
 - Language:English
 - Abstract: BACKGROUND: Mucus hypersecretion from airway epithelium is a characteristic feature of airway inflammatory diseases. Tumor necrosis factor α (TNF-α) 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-α 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 µg/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-α 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-α. CONCLUSION: Our findings demonstrated that MF and BUD attenuated mucin and TNF-α production in PMA-induced human airway epithelial cells.
 
            