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首页> 外文期刊>Cellular Physiology and Biochemistry >Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Mouse Transformed Clara Cells
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Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Mouse Transformed Clara Cells

机译：脂多糖诱导的环氧合酶-2在小鼠转化克拉拉细胞中的表达

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Background/Aims Exacerbation of innate immune responses can contribute to development of acute lung injury. Multiple cell populations, including the bronchiolar epithelium, coordinate these inflammatory responses. Clara cells, non-ciliated epithelial cells, are located in the distal airways in humans and conducting airways in mice. These cells actively participate in innate immune responses but their precise contributions remain poorly defined. Methods To test the hypothesis that iE. coli/i lipopolysaccaride (LPS) treatment stimulates production of pro-inflammatory mediators in mouse transformed Clara cells (MTCC), MTCC were treated with iE. coli/i lipopolysaccaride (LPS). Results LPS increased COX-2 expression and stimulated production of prostaglandins, including prostaglandin Esub2/sub (PGEsub2/sub). Enhanced mitogen activated protein kinase (MAPK) activation, nuclear factor-?B (NF?B) activation, and chemokine production were observed in MTCC in response to LPS treatment. Conclusions While the role for Clara cells in the regulation of host defense and the progression of acute lung injury needs further characterization, our data suggests the importance of this unique cell population in the pathogenesis of LPS-induced acute lung injury.
机译：背景/目的先天免疫反应的加剧可导致急性肺损伤的发展。包括细支气管上皮在内的多个细胞群协调了这些炎症反应。克拉拉细胞（非纤毛上皮细胞）位于人的远端气道中，并在小鼠中传导气道。这些细胞积极参与先天性免疫反应，但其确切的作用仍不清楚。方法检验 E的假设。大肠杆菌脂多糖（LPS）处理刺激小鼠转化的克拉拉细胞（MTCC）中促炎性介质的产生，MTCC用处理。大肠杆菌脂多糖（LPS）。结果脂多糖可增加COX-2的表达并刺激前列腺素的产生，其中包括前列腺素E 2 （PGE 2 ）。响应LPS处理，在MTCC中观察到增强的促分裂原活化蛋白激酶（MAPK）活化，核因子-βB（NFβB）活化和趋化因子产生。结论尽管需要进一步表征Clara细胞在调节宿主防御和急性肺损伤进展中的作用，但我们的数据表明，这种独特的细胞群在LPS诱导的急性肺损伤的发病机理中具有重要意义。

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