The Laryngoscope · 2015
Dexamethasone modulation of MUC5AC and MUC2 gene expression in a generalized model of middle ear inflammation.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Kerschner Joseph E, Khampang Pawjai, Hong Wenzhou
Аннотация
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.
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.