NDLI: TLR4 Signaling augments monocyte chemotaxis by regulating G protein-coupled receptor kinase 2 translocation.

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TLR4 Signaling augments monocyte chemotaxis by regulating G protein-coupled receptor kinase 2 translocation.

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TLR4 Signaling augments monocyte chemotaxis by regulating G protein-coupled receptor kinase 2 translocation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jiang, Yong Fan, Liyan Fan, Jie Li, Song Billiar, Timothy R. Scott, Melanie J. Li, Yuehua Xiao, Guozhi Wang, Juan Liu, Zheng Wilson, Mark A.
Description	Country affiliation: China Author Affiliation: Liu Z ( Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.)
Abstract	Monocytes are critical effector cells of the innate immune system that protect the host by migrating to inflammatory sites, differentiating to macrophages and dendritic cells, eliciting immune responses, and killing pathogenic microbes. MCP-1, also known as CCL2, plays an important role in monocyte activation and migration. The chemotactic function of MCP-1 is mediated by binding to the CCR2 receptor, a member of the G protein-coupled receptor (GPCR) family. Desensitization of GPCR chemokine receptors is an important regulator of the intensity and duration of chemokine stimulation. GPCR kinases (GRKs) induce GPCR phosphorylation, and this leads to GPCR desensitization. Regulation of subcellular localization of GRKs is considered an important early regulatory mechanism of GRK function and subsequent GPCR desensitization. Chemokines and LPS are both present during Gram-negative bacterial infection, and LPS often synergistically exaggerates leukocyte migration in response to chemokines. In this study, we investigated the role and mechanism of LPS-TLR4 signaling on the regulation of monocyte chemotaxis. We demonstrate that LPS augments MCP-1-induced monocyte migration. We also show that LPS, through p38 MAPK signaling, induces phosphorylation of GRK2 at serine 670, which, in turn, suppresses GRK2 translocation to the membrane, thereby preventing GRK2-initiated internalization and desensitization of CCR2 in response to MCP-1. This results in enhanced monocyte migration. These findings reveal a novel function for TLR4 signaling in promoting innate immune cell migration.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300790
Journal	The Journal of Immunology
Issue Number	2
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chemokine Ccl2 Metabolism Chemotaxis, Leukocyte Physiology G-protein-coupled Receptor Kinase 2 Receptors, Ccr2 Toll-like Receptor 4 Animals Anthracenes Pharmacology Bone Marrow Cells Cell Movement Cells, Cultured Immunology Extracellular Signal-regulated Map Kinases Antagonists & Inhibitors Flavonoids Genetics Imidazoles Jnk Mitogen-activated Protein Kinases Lipopolysaccharides Map Kinase Signaling System Macrophages Mice Mice, Inbred C57bl Mice, Knockout Models, Immunological Phosphorylation Pyridines Rna Interference Rna, Small Interfering Deficiency P38 Mitogen-activated Protein Kinases Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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