Joseph E Kerschner1,2, Pawjai Khampang2, Wenzhou Hong2. 1. Division of Pediatric Otolaryngology , Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin, U.S.A. 2. Department of Otolaryngology and Communication Sciences , Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin, U.S.A.
Abstract
OBJECTIVES/HYPOTHESIS: To examine the effect of dexamethasone on basal and proinflammatory cytokine-induced gel-forming mucin expression in human middle ear epithelial cell line (HMEEC-1). METHODS: HMEEC-1 was exposed to proinflammatory cytokines, tumor necrosis factor-alpha (TNF-), and interleukin-1 beta (IL-1β) to identify optimal mucin induction. The HMEEC-1 was incubated with dexamethasone in the steady state and in the presence of proinflammatory cytokine stimulation. Expression of MUC2 and MUC5AC was determined by quantitative polymerase chain reaction. RESULTS: Proinflammatory cytokines, TNF-α and IL-1β, induced MUC2 and MUC5AC expression in HMEEC-1. Dexamethasone reduced steady state mRNA level of MUC5AC in a time-dependent (P < 0.05) and dose-dependent (P < 0.0001) manner. MUC2 was effectively suppressed at all time points tested (P < 0.05). Temporal difference between dexamethasone suppression of MUC2 and MUC5AC was demonstrated. Dexamethasone inhibits the proinflammatory cytokine-induced expression of both MUC2 and MUC5AC. CONCLUSION: This work provides a conclusive picture of the ability of using glucocorticoids to downregulate mucin gene expression in human MEE using a generalizable model of inflammation that is applicable to multiple potential causes of MEE mucosal hypertrophy. This data adds to the promising potential of future interventions for patients with chronic otitis media. LEVEL OF EVIDENCE: N/A. Laryngoscope, 126:E248-E254, 2016.
OBJECTIVES/HYPOTHESIS: To examine the effect of dexamethasone on basal and proinflammatory cytokine-induced gel-forming mucin expression in human middle ear epithelial cell line (HMEEC-1). METHODS:HMEEC-1 was exposed to proinflammatory cytokines, tumor necrosis factor-alpha (TNF-), and interleukin-1 beta (IL-1β) to identify optimal mucin induction. The HMEEC-1 was incubated with dexamethasone in the steady state and in the presence of proinflammatory cytokine stimulation. Expression of MUC2 and MUC5AC was determined by quantitative polymerase chain reaction. RESULTS: Proinflammatory cytokines, TNF-α and IL-1β, induced MUC2 and MUC5AC expression in HMEEC-1. Dexamethasone reduced steady state mRNA level of MUC5AC in a time-dependent (P < 0.05) and dose-dependent (P < 0.0001) manner. MUC2 was effectively suppressed at all time points tested (P < 0.05). Temporal difference between dexamethasone suppression of MUC2 and MUC5AC was demonstrated. Dexamethasone inhibits the proinflammatory cytokine-induced expression of both MUC2 and MUC5AC. CONCLUSION: This work provides a conclusive picture of the ability of using glucocorticoids to downregulate mucin gene expression in human MEE using a generalizable model of inflammation that is applicable to multiple potential causes of MEE mucosal hypertrophy. This data adds to the promising potential of future interventions for patients with chronic otitis media. LEVEL OF EVIDENCE: N/A. Laryngoscope, 126:E248-E254, 2016.
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