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首页> 外文期刊>American Journal of Physiology >Ultrafine carbon particles induce interleukin-8 gene transcription and p38 MAPK activation in normal human bronchial epithelial cells.
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Ultrafine carbon particles induce interleukin-8 gene transcription and p38 MAPK activation in normal human bronchial epithelial cells.

机译：超细碳颗粒在正常人支气管上皮细胞中诱导白介素8基因转录和p38 MAPK活化。

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摘要

Epidemiological studies suggest that ultrafine particles contribute to particulate matter-induced adverse health effects. Interleukin (IL)-8 is an important proinflammatory cytokine in the human lung that is induced in respiratory cells exposed to a variety of environmental insults, including ambient air ultrafine particles. In this study, we examined the effect of a model ultrafine particle on IL-8 expression and the cellular mechanisms responsible for this event. Here, we report that carbonaceous ultrafine particles consisting of synthetic elemental carbon particles (UfCP) markedly increase the expression of IL-8 mRNA and protein in normal human bronchial epithelial (NHBE) cells. IL-8 promoter activity was increased by UfCP exposure in NHBE cells, indicating UfCP-induced IL-8 expression is transcriptionally regulated. IL-8 expression in NHBE is known to be regulated by nuclear factor (NF)-kappaB activation. However, UfCP did not induce inhibitory factor kappaBalpha degradation, NF-kappaB-DNA binding,or NF-kappaB-dependent promoter activity in NHBE cells, indicating that UfCP induces IL-8 expression through a mechanism that is independent of NF-kappaB activation. Additionally, we observed that UfCP exposure induces the phosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) in a biphasic manner and that the inhibition of p38 MAPK activity can block IL-8 mRNA expression induced by UfCP in NHBE cells. These results demonstrate that UfCP-induced expression of IL-8 involves a transcriptional mechanism and activation of p38 MAPK in NHBE cells.
机译：流行病学研究表明，超细颗粒有助于颗粒物引起的不利健康影响。白介素（IL）-8是人肺中一种重要的促炎细胞因子，在暴露于各种环境损害（包括环境空气超细颗粒）的呼吸细胞中被诱导。在这项研究中，我们检查了模型超细颗粒对IL-8表达的影响以及引起该事件的细胞机制。在这里，我们报道由合成元素碳颗粒（UfCP）组成的碳质超细颗粒显着增加正常人支气管上皮（NHBE）细胞中IL-8 mRNA和蛋白质的表达。通过在NHBE细胞中暴露于UfCP，IL-8启动子活性增加，表明UfCP诱导的IL-8表达受到转录调节。已知NHBE中的IL-8表达受核因子（NF）-κB激活的调节。但是，UfCP不会在NHBE细胞中诱导抑制因子kappaBalpha降解，NF-kappaB-DNA结合或NF-kappaB依赖的启动子活性，表明UfCP通过独立于NF-kappaB激活的机制诱导IL-8表达。此外，我们观察到UfCP暴露以双相方式诱导p38丝裂原活化蛋白激酶（MAPK）的磷酸化和激活，并且p38 MAPK活性的抑制可以阻断UfCP在NHBE细胞中诱导的IL-8 mRNA表达。这些结果表明，UfCP诱导的IL-8表达涉及NHBE细胞中的转录机制和p38 MAPK的激活。

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