Inoue Ken-ichiro, Takano Hirohisa, Yanagisawa Rie, Hirano Seishiro, Kobayashi Takahiro, Ichinose Takamichi, Yoshikawa Toshikazu
Environmental Health Sciences Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba 305-8506 Ibaraki, Japan.
Arch Toxicol. 2006 Dec;80(12):833-8. doi: 10.1007/s00204-006-0105-1.
The effects of components of ambient particulate matter (PM) on individuals with predisposing respiratory disorders are not well defined. We have previously demonstrated that airway exposure to diesel exhaust particles (DEP) or organic chemicals (OC) extracted from DEP (DEP-OC) enhances lung inflammation related to bacterial endotoxin (lipopolysaccharide, LPS). The present study aimed to examine the effects of airway exposure to OC extracted from urban PM (PM-OC) on lung inflammation related to LPS. ICR mice were divided into four experimental groups that intratracheally received vehicle, LPS (2.5 mg/kg), PM-OC (4 mg/kg), or PM-OC + LPS. Lung inflammation, lung water content, and lung expression of cytokines were evaluated 24 h after intratracheal administration. LPS challenge elicited lung inflammation evidenced by cellular profiles of bronchoalveolar lavage fluid and lung histology, which was further aggravated by the combined challenge with PM-OC. The combination with PM-OC and LPS did not significantly exaggerate LPS-elicited pulmonary edema. LPS instillation induced elevated lung expression of interleukin-1beta, macrophage inflammatory protein-1alpha, macrophage chemoattractant protein-1, and keratinocyte chemoattractant, whereas the combined challenge with PM-OC did not influence these levels. All the results were consistent with our previous reports on DEP-OC. These results suggest that the extracted organic chemicals from PM exacerbate infectious lung inflammation. The mechanisms underlying the enhancing effects are not mediated via the enhanced local expression of proinflammatory cytokines.
环境颗粒物（PM）成分对易患呼吸道疾病个体的影响尚不明确。我们之前已经证明，气道暴露于柴油废气颗粒（DEP）或从DEP中提取的有机化学物质（DEP-OC）会加剧与细菌内毒素（脂多糖，LPS）相关的肺部炎症。本研究旨在探讨气道暴露于从城市PM中提取的OC（PM-OC）对与LPS相关的肺部炎症的影响。将ICR小鼠分为四个实验组，分别经气管内给予载体、LPS（2.5mg/kg）、PM-OC（4mg/kg）或PM-OC+LPS。在气管内给药24小时后评估肺部炎症、肺含水量和细胞因子的肺表达。LPS激发引起肺部炎症，通过支气管肺泡灌洗液的细胞图谱和肺组织学得以证明，PM-OC联合激发进一步加剧了这种炎症。PM-OC与LPS联合使用并未显著加剧LPS引起的肺水肿。LPS滴注诱导白细胞介素-1β、巨噬细胞炎性蛋白-1α、巨噬细胞趋化蛋白-1和角质形成细胞趋化因子的肺表达升高，而PM-OC联合激发并未影响这些水平。所有结果与我们之前关于DEP-OC的报道一致。这些结果表明，从PM中提取的有机化学物质会加剧感染性肺部炎症。增强作用的潜在机制并非通过促炎细胞因子的局部表达增强来介导。
