An essential role for RIG-I in toll-like receptor-stimulated phagocytosis

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 ex...

Full description

Saved in:
Bibliographic Details
Published in:Cell host & microbe 2009-08, Vol.6 (2), p.150-161
Main Authors: 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
Format: Article
Language:English
Subjects:
Actin-Related Protein 2-3 Complex - metabolism
Animals
Cell Line
DEAD Box Protein 58
DEAD-box RNA Helicases - genetics
DEAD-box RNA Helicases - immunology
Escherichia coli - immunology
Escherichia coli Infections - immunology
Gene Silencing
GTPase-Activating Proteins - metabolism
Macrophages - microbiology
Mice
Mice, Knockout
Neuropeptides - metabolism
Phagocytosis - immunology
rac GTP-Binding Proteins - metabolism
rac1 GTP-Binding Protein
RNA, Small Interfering - genetics
RNA, Small Interfering - metabolism
Survival Analysis
Toll-Like Receptor 4 - immunology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1931-3128
1934-6069
DOI:10.1016/j.chom.2009.06.008