Fluticasone and budesonide inhibit cytokine release in human lung epithelial cells and alveolar macrophages
作者： A Ek , K Larsson , S Siljerud , L Palmberg
DOI: 10.1034/J.1398-9995.1999.00087.X
关键词: Cytokine secretion 、 Fluticasone 、 Internal medicine 、 Proinflammatory cytokine 、 Biology 、 Pulmonary alveolus 、 Endocrinology 、 Interleukin 8 、 A549 cell 、 Cytokine 、 Interleukin 6
摘要: Glucocorticoids are potent anti-inflammatory agents capable of influencing cytokine release in a number cell types. The aim the present study was to investigate whether glucocorticoids, frequently used treatment asthma, interfere with secretion by lung epithelial cells and alveolar macrophages vitro. Inhalation swine dust induces airway inflammation influx inflammatory proinflammatory cytokines lungs. Therefore, human (A549) were stimulated or lipopolysaccharide (LPS), inhibitory effect budesonide fluticasone propionate on studied dose-response (10(-13)-10(-8) M) manner. time course for steroid also investigated. Both steroids caused dose-dependent, almost total, inhibition dust-induced IL-6 IL-8 from LPS-induced TNF-alpha macrophages. only partially inhibited Budesonide approximately 10 times less than propionate. Preincubation did not inhibit more simultaneous incubation stimulus steroid. In conclusion, propionate, concentrations that probably occur lining fluid during inhalational therapy, (IL-6, IL-8) (TNF-alpha, IL-6, IL-8). vitro, onset this rapid.
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