Postlethwait Edward M
Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, Birmingham, AL 35294-0022, USA.
J Clin Invest. 2007 Mar;117(3):601-4. doi: 10.1172/JCI31549.
Inhaled environmental oxidants, such as ozone and particulates, have been variably linked to epithelial injury, inflammation, and perturbations in lung development, growth, and function. Reactions between ozone and lung surface lipids likely account for exposure-related pathophysiologic sequelae. In this issue of the JCI, Dahl et al. document a previously unrecognized pulmonary defense against inhaled oxidants in mice: macrophage scavenger receptors (SRs) bind proinflammatory oxidized lipids, thereby decreasing pulmonary inflammation (see the related article beginning on page 757). The study adds to our knowledge of diverse lung oxidative processes and identifies a potential regulatory mechanism governing pulmonary inflammation. Further investigations to elucidate more precise mechanisms and to determine the influence of SRs on airway epithelial injury, repair, and remodeling are warranted.
吸入性环境氧化剂，如臭氧和颗粒物，与上皮损伤、炎症以及肺发育、生长和功能的紊乱存在不同程度的关联。臭氧与肺表面脂质之间的反应可能是暴露相关病理生理后遗症的原因。在本期《临床研究杂志》中，达尔等人记录了小鼠中一种先前未被认识的针对吸入性氧化剂的肺部防御机制：巨噬细胞清道夫受体（SRs）结合促炎性氧化脂质，从而减轻肺部炎症（见第757页开始的相关文章）。这项研究增加了我们对多种肺部氧化过程的了解，并确定了一种控制肺部炎症的潜在调节机制。有必要进一步开展研究，以阐明更精确的机制，并确定SRs对气道上皮损伤、修复和重塑的影响。
