Ultrastructural changes of the air-blood barrier in mice after intratracheal instillation of lipopolysaccharide and ultrafine carbon black particles
Ultrastructural changes of the air-blood barrier in mice after intratracheal instillation of lipopolysaccharide and ultrafine carbon black particles
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DOI：
10.1016/j.etp.2007.10.001
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发表时间：
2009-01-01
影响因子：
--
通讯作者：
Takano, Hirohisa
中科院分区：
文献类型：
--
作者：
Inoue, Hiromi;Shimada, Akinori;Takano, Hirohisa
流行病学研究表明，暴露于环境超细颗粒物浓度增加与特别是易感个体的不良健康影响之间存在关联。为阐明脂多糖（LPS）致急性肺损伤的机制，采用经气管内滴注超细炭黑（UFCB）的方法，观察UFCB从肺到体循环的转运途径。此外，还用电镜观察了LPS和UFCB肺内滴注所致的肺毒性。LPS处理诱导急性炎症变化，在变性的肺泡壁中活化的巨噬细胞和中性粒细胞的数量增加。UFCB出现在气-血屏障基底膜上或基底膜内，与肺泡1型上皮细胞胞浆的水肿和碎裂有关，肺泡1型上皮细胞的损伤常发生在UFCB团块附近。这些结果表明，暴露的超细颗粒物的移位可能会在急性炎症变化的肺组织中增强。(C)2007年爱思唯尔有限公司。All rights reserved.
Epidemiological studies have indicated associations between exposure to increased concentrations of ambient Ultrafine particles and adverse health effects especially in susceptible individuals. To ellucidate the mechanisms Underlying the findings from epidemiological studies, mice pretreated with lipopolysaccharide (LPS) (acute lung injury model) were intratracheally instilled with Ultrafine carbon black particles (UFCB), and the air-blood barrier was observed to examine the translocation pathway of UFCB front the lung into the systemic Circulation. In addition, lung toxicity induced by the intratracheal instillation of LPS and UFCB was Studied with the use of electron microscope. LPS treatment induced acute inflammatory changes with increased number of activated macrophages and neutrophils in the degenerated alveolar walls. UFCB were demonstrated on or in the denuded basement membrane In the air-blood barrier: these findings were associated with edematous changes and fragmentation of the cytoplasms of alveolar epithelial cell type 1, and the damages of alveolar epithelial cell type 1 were frequently observed in the close vicinity of the clumps of UFCB. These findings suggest that translocation of the exposed ultrafine particles may be enhanced in the lung tissues with acute inflammatory changes. (C) 2007 Elsevier GmbH. All rights reserved.