Organic compounds from diesel exhaust particles elicit a proinflammatory response in human airway epithelial cells and induce cytochrome p450 1A1 expression
Organic compounds from diesel exhaust particles elicit a proinflammatory response in human airway epithelial cells and induce cytochrome p450 1A1 expression
复制标题
DOI：
10.1165/ajrcmb.25.4.4515
复制
发表时间：
2001-10-01
影响因子：
6.4
通讯作者：
Marano, F
中科院分区：
文献类型：
--
作者：
Bonvallot, V;Baeza-Squiban, A;Marano, F
已知柴油机排气颗粒（DEP）增强人类志愿者的炎症反应。在培养的人支气管上皮（16 HBE）细胞中，它们在触发转导途径（包括核因子（NF）-KB活化和丝裂原活化蛋白激酶（MAPK）磷酸化）后诱导促炎细胞因子的释放。本研究比较了天然DEP（nDEP），DEP的有机提取物（OE-DEP），以及以剥离DEP（sDEP）和炭黑颗粒（CB）为代表的碳质颗粒的效果，以阐明它们各自的作用。OE-DEP和nDEP诱导粒细胞巨噬细胞集落刺激因子（GM-CSF）释放、NF-κ B活化和MAPK磷酸化。碳质核心通常引起较不强烈的影响。活性氧在16 HBE细胞中产生，并参与GM-CSF的释放和nDEP和OE-DEP对NF-κ B DNA结合的刺激。我们证明，第一次，在气道上皮细胞在体外，nDEP诱导CYP 1A 1，细胞色素P450的表达，特别是参与多环芳烃代谢，从而证明了有机化合物在DEP诱导的促炎反应的关键作用。了解DEP组分在这些影响中的各自贡献对于车辆制造商来说非常重要，以便改进其废气后处理技术。总之，DEP诱导的气道上皮细胞炎症反应主要涉及有机化合物如PAH，其诱导CYP 1A 1基因表达。
Diesel exhaust particles (DEP) are known to enhance inflammatory responses in human volunteers. In cultured human bronchial epithelial (16HBE) cells, they induce the release of proinflammatory cytokines after triggering transduction pathways, including nuclear factor (NF)-KB activation and mitogen-activated protein kinase (MAPK) phosphorylation. This study compares the effects of native DEP (nDEP), organic extracts of DEP (OE-DEP), and carbonaceous particles, represented by stripped DEP (sDEP) and carbon black particles (CB), in order to clarify their respective roles. OE-DEP and nDEP induce granulocyte macrophage colony-stimulating factor (GM-CSF) release, NF-KB activation, and MAPK phosphorylation. The carbonaceous core generally induces less intense effects. Reactive oxygen species are produced in 16HBE cells and are involved in GM-CSF release and in the stimulation of NF-KB DNA binding by nDEP and OE-DEP. We demonstrate, for the first time, in airway epithelial cells in vitro that nDEP induce the expression of the CYP1A1, a cytochrome P450 specifically involved in polycyclic aromatic hydrocarbons metabolism, thereby demonstrating the critical role of organic compounds in the DEP-induced proinflammatory response. Understanding the respective contributions of DEP components in these effects is important for vehicle manufacturers in order to improve their exhaust gas post-treatment technologies. In conclusion, the DEP-induced inflammatory response in airway epithelial cells mainly involves organic compounds such as PAH, which induce CYP1A1 gene expression.