Kong Ling, Sun Lei, Zhang Hongxin, Liu Qin, Liu Ye, Qin Linhua, Shi Guojun, Hu Jun-Hao, Xu Ajing, Sun Yue-Ping, Li Dangsheng, Shi Yu-Fang, Zang Jing-Wu, Zhu Jiang, Chen Zhu, Wang Zhu-Gang, Ge Bao-Xue
The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai JiaoTong University School of Medicine, Shanghai 200025, China.
Cell Host Microbe. 2009 Aug 20;6(2):150-61. doi: 10.1016/j.chom.2009.06.008.
Retinoic acid-inducible gene-I (RIG-I) plays an important role in antiviral response by recognizing double-stranded RNA. Here we demonstrate an unanticipated role of RIG-I in Toll-like receptor (TLR)-stimulated phagocytosis. Stimulation with lipopolysaccharide (LPS), a ligand of TLR4, induced the expression of RIG-I in macrophages. Depletion of RIG-I by RNAi or gene targeting inhibited the LPS-induced phagocytosis of bacteria. Cellular processes involved in phagocytosis, such as small GTPase Cdc42/Rac1 activation, actin polymerization, and actin-regulator Arp2/3 recruitment, were also impaired in RIG-I-deficient macrophages activated by LPS. Moreover, RIG-I(-/-) mice were found to be more susceptible to infection with Escherichia coli as compared to wild-type mice. Thus, the regulatory functions of RIG-I are strikingly broad, including a role not only in antiviral responses but in antibacterial responses as well.
视黄酸诱导基因I（RIG-I）通过识别双链RNA在抗病毒反应中发挥重要作用。在此，我们证明了RIG-I在Toll样受体（TLR）刺激的吞噬作用中具有意想不到的作用。用TLR4的配体脂多糖（LPS）刺激可诱导巨噬细胞中RIG-I的表达。通过RNA干扰或基因靶向缺失RIG-I可抑制LPS诱导的细菌吞噬作用。在LPS激活的RIG-I缺陷巨噬细胞中，参与吞噬作用的细胞过程，如小GTP酶Cdc42/Rac1激活、肌动蛋白聚合和肌动蛋白调节因子Arp2/3募集，也受到损害。此外，与野生型小鼠相比，发现RIG-I（-/-）小鼠对大肠杆菌感染更敏感。因此，RIG-I的调节功能非常广泛，不仅在抗病毒反应中起作用，在抗菌反应中也起作用。
