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Diesel exhaust particles increase IL-1β-induced human β-defensin expression via NF-κB-mediated pathway in human lung epithelial cells

机译:柴油机排气颗粒通过人肺上皮细胞中的NF-κB介导的途径增加IL-1β诱导的人β-防御素表达

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摘要

BackgroundHuman β-defensin (hBD)-2, antimicrobial peptide primarily induced in epithelial cells, is a key factor in the innate immune response of the respiratory tract. Several studies showed increased defensin levels in both inflammatory lung diseases, such as cystic fibrosis, diffuse panbronchiolitis, idiopathic pulmonary fibrosis and acute respiratory distress syndrome, and infectious diseases. Recently, epidemiologic studies have demonstrated acute and serious adverse effects of particulate air pollution on respiratory health, especially in people with pre-existing inflammatory lung disease. To elucidate the effect of diesel exhaust particles (DEP) on pulmonary innate immune response, we investigated the hBD-2 and interleukin-8 (IL-8) expression to DEP exposure in interleukin-1 beta (IL-1β)-stimulated A549 cells.
机译:背景人类β-防御素(hBD)-2是主要在上皮细胞中诱导的抗菌肽,是呼吸道先天免疫反应的关键因素。几项研究表明,在两种炎症性肺病(如囊性纤维化,弥漫性全细支气管炎,特发性肺纤维化和急性呼吸窘迫综合征)和感染性疾病中,防御素水平均升高。最近,流行病学研究表明,颗粒空气污染对呼吸系统健康有严重的严重影响,尤其是对于已患有炎症性肺病的人。为了阐明柴油机排气颗粒(DEP)对肺部固有免疫反应的影响,我们研究了IL-1β(IL-1β)刺激的A549细胞中hBD-2和白细胞介素8(IL-8)表达对DEP暴露的影响。

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