The macrophage scavenger receptor SR-AI/II and lung defense against pneumococci and particles
The macrophage scavenger receptor SR-AI/II and lung defense against pneumococci and particles
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DOI：
10.1165/rcmb.2006-0128oc
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发表时间：
2006-10-01
影响因子：
6.4
通讯作者：
Kobzik, Lester
中科院分区：
文献类型：
--
作者：
Arredouani, Mohamed S.;Yang, Zhiping;Kobzik, Lester
A类巨噬细胞清道夫受体SR-AI/II被认为是先天免疫的模式识别受体，但其在肺防御中的功能作用尚未研究。我们使用SR-AI/II基因缺陷的小鼠及其野生型C57 BL/6对应物来研究这种受体对防御肺炎球菌感染和吸入颗粒的贡献。SR-AI/II缺陷导致体内荧光细菌的吞噬作用受损，减少了肺中活细菌的清除，并大大增加了肺炎。生存研究还显示，肺炎球菌肺部感染的SR-AI/II-基因型小鼠的死亡率增加。类似地，在用TiO 2颗粒激发气道后，SR-AI/II缺陷小鼠在肺灌洗液中显示出促炎细胞因子水平增加和更明显的嗜酸性炎症。这些数据表明，肺巨噬细胞A类清道夫受体SR-AI/II有助于对细菌和吸入颗粒的先天防御。
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-cleficient mice with pneumococcal lung infection. Similarly, after challenge of the airways with TiO2 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.