Arredouani Mohamed S, Yang Zhiping, Imrich Amy, Ning Yaoyu, Qin Guozhong, Kobzik Lester
Physiology Program, 665 Huntington Avenue, SPH-II, Room 221, Boston, MA 02115, USA.
Am J Respir Cell Mol Biol. 2006 Oct;35(4):474-8. doi: 10.1165/rcmb.2006-0128OC. Epub 2006 May 4.
The class A macrophage scavenger receptor SR-AI/II is implicated as a pattern recognition receptor for innate immunity, but its functional role in lung defense has not been studied. We used mice genetically deficient in SR-AI/II and their wild-type C57BL/6 counterparts to investigate the contribution of this receptor to defense against pneumococcal infection and inhaled particles. SR-AI/II deficiency caused impaired phagocytosis of fluorescent bacteria in vivo, diminished clearance of live bacteria from the lungs, and substantially increased pneumonic inflammation. Survival studies also showed increased mortality in SR-AI/II-deficient mice with pneumococcal lung infection. Similarly, after challenge of the airways with TiO(2) particles, SR-AI/II-deficient mice showed increased proinflammatory cytokine levels in lung lavage fluid and a more pronounced neutrophilic inflammation. The data indicate that the lung macrophage class A scavenger receptor SR-AI/II contributes to innate defense against bacteria and inhaled particles.
A类巨噬细胞清道夫受体SR-AI/II被认为是一种参与固有免疫的模式识别受体,但其在肺部防御中的功能作用尚未得到研究。我们使用基因敲除SR-AI/II的小鼠及其野生型C57BL/6对照小鼠,来研究该受体在抵御肺炎球菌感染和吸入颗粒方面的作用。SR-AI/II基因缺陷导致体内荧光细菌的吞噬作用受损,肺部活菌清除能力下降,并显著加剧肺部炎症。生存研究还显示,患有肺炎球菌肺部感染的SR-AI/II基因缺陷小鼠死亡率增加。同样,在用TiO(2)颗粒攻击气道后,SR-AI/II基因缺陷小鼠肺灌洗液中的促炎细胞因子水平升高,中性粒细胞炎症更为明显。这些数据表明,肺部巨噬细胞A类清道夫受体SR-AI/II有助于对细菌和吸入颗粒的固有防御。