Exposure to environmental tobacco smoke induces angiogenesis and leukocyte trafficking in lung microvessels.

Exposure to environmental tobacco smoke induces angiogenesis and leukocyte trafficking in lung microvessels.
复制标题

暴露于环境烟草烟雾会诱导肺微血管中的血管生成和白细胞贩运。

DOI:
10.1080/01902140802449729
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发表时间:
2009
影响因子:
1.7
通讯作者:
Sriramarao,P
Sriramarao,P
中科院分区:
医学4区
文献类型:
--
作者:
Rao,SavitaP;Sikora,Lyudmila;Hosseinkhani,MReza;Pinkerton,KentE;Sriramarao,P

文献摘要

相似文献

已知暴露于环境烟草烟雾(ETS)会导致和加剧肺部炎症性疾病,如慢性阻塞性肺疾病(COPD)和哮喘。研究了ETS对促进肺部炎症的血管生成和白细胞募集的影响,将暴露于老化和稀释的侧流香烟烟雾或新鲜空气中12周的小鼠肺组织移植到裸鼠背部皮肤褶腔中。通过活体显微镜观察,与暴露于新鲜空气中的肺组织相比,暴露于香烟烟雾12周的小鼠肺组织显示出血管密度(血管生成)显著增加,这与选择素介导的血管内白细胞滚动和粘附增加有关。此外,与尼古丁暴露小鼠肺微血管中的对照组中性粒细胞相比,尼古丁暴露小鼠的中性粒细胞显示出明显增加的滚动和粘附性,这表明香烟烟雾中的尼古丁可以增强白细胞与内皮细胞的相互作用。ets诱导的血管生成和白细胞运输可能在ets相关疾病(如COPD支气管炎或哮喘)的气道炎症细胞募集中发挥关键作用。
Exposure to environmental tobacco smoke (ETS) is known to contribute to and exacerbate inflammatory diseases of the lung such as chronic obstructive pulmonary disease (COPD) and asthma. The effect of ETS on angiogenesis and leukocyte recruitment, both of which promote lung inflammation, was investigated using lung tissue from mice exposed to aged and diluted sidestream cigarette smoke or fresh air for 12 weeks and transplanted into dorsal skin-fold chambers in nude mice. Lung tissue from mice exposed to cigarette smoke for 12 weeks exhibited significantly increased vascular density (angiogenesis) associated with selectin-mediated increased intravascular leukocyte rolling and adhesion compared to fresh air–exposed lung tissue by intravital microscopy. Further, neutrophils from nicotine-exposed mice displayed significantly increased rolling and adhesion compared to control neutrophils in microvessels of nicotine-exposed lungs versus control lung microvessels, suggesting that nicotine in cigarette smoke can augment leukocyte-endothelial interactions. ETS-induced angiogenesis and leukocyte trafficking may play a key role in airway recruitment of inflammatory cells in ETS-associated disorders such as COPD bronchitis or asthma.