Macrophages, reactive nitrogen species, and lung injury
Macrophages, reactive nitrogen species, and lung injury
复制标题
DOI：
10.1111/j.1749-6632.2010.05607.x
复制
发表时间：
2010-01-01
期刊：
影响因子：
--
通讯作者：
Laskin, Jeffrey D.
中科院分区：
文献类型：
--
作者：
Laskin, Debra L.;Sunil, Vasanthi R.;Laskin, Jeffrey D.
过去几年积累的证据表明，吸入臭氧等刺激物造成的肺损伤不仅是由于这种化学物质的直接影响，也是由渗透的巨噬细胞释放的炎症介质的作用间接造成的。在参与细胞毒性过程的介体中，活性氮物种(RNS)因其潜在的细胞毒性而备受关注。巨噬细胞抑制阻止RNS的产生和臭氧诱导的毒性的发现有力地支持了这些细胞和炎症介质在肺损伤中的作用。最近的研究集中在了解巨噬细胞被激活以释放RNS的途径。一种引起相当大关注的蛋白质是小窝蛋白-1，这是一种膜支架分子，其功能是负向调节细胞信号。吸入臭氧后巨噬细胞中小窝蛋白-1的表达下调，这一事实表明了控制这些炎症细胞释放细胞毒性介质的机制。
Evidence has accumulated over the past several years demonstrating that lung injury following inhalation of irritants like ozone is due, not only to direct effects of the chemical, but also indirectly to the actions of inflammatory mediators released by infiltrating macrophages. Among the mediators involved in the cytotoxic process, reactive nitrogen species (RNS) are of particular interest because of their well-documented cytotoxic potential. Findings that macrophage suppression blocks RNS production and ozone-induced toxicity provide strong support for a role of these cells and inflammatory mediators in lung injury. Recent investigations have focused on understanding pathways by which macrophages become activated to release RNS. One protein that has attracted considerable attention is caveolin-1, a membrane scaffolding molecule that functions to negatively regulate cell signaling. The fact that expression of caveolin-1 is down-regulated in macrophages after ozone inhalation suggests a mechanism controlling the release of cytotoxic mediators by these inflammatory cells.