Responses of well-differentiated nasal epithelial cells exposed to particles: Role of the epithelium in airway inflammation
Responses of well-differentiated nasal epithelial cells exposed to particles: Role of the epithelium in airway inflammation
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DOI：
10.1016/j.taap.2006.03.002
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发表时间：
2006-09-15
影响因子：
3.8
通讯作者：
Dazy, Anne-Catherine
中科院分区：
文献类型：
--
作者：
Auger, Floriane;Gendron, Marie-Claude;Dazy, Anne-Catherine
大量流行病学研究支持这样一种观点，即环境空气污染颗粒会对人类健康产生不利影响。为了解释暴露于颗粒的气道中的急性炎症过程，已经对浸没在塑料和低分化细胞上生长的细胞以及细胞系进行了许多体外研究，这些细胞系的生理学与良好分化的细胞有所不同。为了获得与人体气道相似的模型系统的结果，在气液界面（ALI）中培养的分化良好的人鼻上皮（HNE）细胞的顶膜暴露于柴油废气颗粒（DEP）和巴黎城市空气颗粒（PM2.5）中24小时。DEP和PM2.5 （10-80 μ g/cm(2)）均刺激IL-8和双调节蛋白（EGFR配体）仅向基底室分泌。相比之下，没有IL-1 β分泌，只有微弱的不可复制的tnf - α分泌。只有当细胞暴露于PM2.5时，IL-6和GM-CSF才会持续向根尖室刺激。颗粒暴露后细胞表面的icam - 1蛋白表达仍然很低，但tnf - α处理后细胞表面的icam - 1蛋白表达增加。颗粒内化被认为会引发氧化应激和促炎细胞因子的表达，但仅限于小颗粒颗粒(
Numerous epidemiological studies support the contention that ambient air pollution particles can adversely affect human health. To explain the acute inflammatory process in airways exposed to particles, a number of in vitro studies have been performed on cells grown submerged on plastic and poorly differentiated, and on cell lines, the physiology of which is somewhat different from that of well-differentiated cells. In order to obtain results using a model system in which epithelia] cells are similar to those of the human airway in vivo, apical membranes of well-differentiated human nasal epithelial (HNE) cells cultured in an air-liquid interface (ALI) were exposed for 24 h to diesel exhaust particles (DEP) and Paris urban air particles (PM2.5). DEP and PM2.5 (10-80 mu g/cm(2)) stimulated both IL-8 and amphiregulin (ligand of EGFR) secretion exclusively towards the basal compartment. In contrast, there was no IL-1 beta secretion and only weak non-reproducible secretion of TNF-alpha. IL-6 and GM-CSF were consistently stimulated towards the apical compartment and only when cells were exposed to PM2.5. ICAM-I protein expression on cell surfaces remained low after particle exposure, although it increased after TNF-alpha treatment. Internalization of particles, which is believed to initiate oxidative stress and proinflammatory cytokine expression, was restricted to small nanoparticles (