Allergen-induced IL-9 directly stimulates mucin transcription in respiratory epithelial cells
Allergen-induced IL-9 directly stimulates mucin transcription in respiratory epithelial cells
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DOI：
10.1172/jci6097
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发表时间：
1999-11-01
影响因子：
15.9
通讯作者：
Basbaum, C
中科院分区：
文献类型：
--
作者：
Longphre, M;Li, D;Basbaum, C
哮喘的一个标志是粘蛋白过度产生，这种情况会导致气道阻塞。造成粘蛋白过量产生的事件尚不清楚，但被认为与慢性炎症介质有关。其他研究表明，粘液细胞化生需要辅助性 T 2 (Th2) 淋巴细胞，从而导致过敏动物模型中粘蛋白过量产生。我们假设 Th2 细胞介质存在于哮喘气道液中并直接刺激气道上皮细胞中的粘蛋白合成。培养的气道上皮细胞的结果表明，哮喘液体样品刺激粘蛋白（MUCSAC）的合成比非哮喘液体样品有效数倍。与此相一致的是，来自受过敏原挑战的狗气道的灌洗液刺激粘蛋白合成的效果比来自未受过敏原挑战的狗强几倍。狗样本的分级显示出 2 个活性组分
A hallmark of asthma is mucin overproduction, a condition that contributes to airway obstruction. The events responsible for mucin overproduction are not known but are thought to be associated with mediators of chronic inflammation. Others have shown that T-helper 2 (Th2) lymphocytes are required for mucous cell metaplasia, which then leads to mucin overproduction in animal models of allergy. We hypothesized that Th2 cell mediators are present in asthmatic airway fluid and directly stimulate mucin synthesis in airway epithelial cells. Results in cultured airway epithelial cells showed that samples of asthmatic fluid stimulated mucin (MUCSAC) synthesis severalfold more potently than non-asthmatic fluid. Consistent with this, lavage fluid from the airways of allergen-challenged dogs stimulated mucin synthesis severalfold more potently than that from non-allergen-challenged dogs. Fractionation of dog samples revealed 2 active fractions at