The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response

Macrophages are crucial members of the mononuclear phagocyte system essential to protect the host from invading pathogens and are central to the inflammatory response with their ability to acquire specialized phenotypes of inflammatory (M1) and anti-inflammatory (M2) and to produce a pool of inflamm...

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Main Authors: Liqian Zhu, Clinton Jones, Gaiping Zhang
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2018/5201759
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author Liqian Zhu
Clinton Jones
Gaiping Zhang
author_facet Liqian Zhu
Clinton Jones
Gaiping Zhang
author_sort Liqian Zhu
collection DOAJ
description Macrophages are crucial members of the mononuclear phagocyte system essential to protect the host from invading pathogens and are central to the inflammatory response with their ability to acquire specialized phenotypes of inflammatory (M1) and anti-inflammatory (M2) and to produce a pool of inflammatory mediators. Equipped with a broad range of receptors, such as Toll-like receptor 4 (TLR4), CD14, and Fc gamma receptors (FcγRs), macrophages can efficiently recognize and phagocytize invading pathogens and secrete cytokines by triggering various secondary signaling pathways. Phospholipase C (PLC) is a family of enzymes that hydrolyze phospholipids, the most significant of which is phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2]. Cleavage at the internal phosphate ester generates two second messengers, inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG), both of which mediate in diverse cellular functions including the inflammatory response. Recent studies have shown that some PLC isoforms are involved in multiple stages in TLR4-, CD14-, and FcγRs-mediated activation of nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and interferon regulatory factors (IRFs), all of which are associated with the regulation of the inflammatory response. Therefore, secondary signaling by PLC is implicated in the pathogenesis of numerous inflammatory diseases. This review provides an overview of our current knowledge on how PLC signaling regulates the macrophage-mediated inflammatory response.
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spelling doaj-art-15e6a49ad7da4dacb6b005ab86bbab862025-02-03T06:07:00ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/52017595201759The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory ResponseLiqian Zhu0Clinton Jones1Gaiping Zhang2College of Veterinary Medicine and Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, 48 Wenhui East Road, Yangzhou, Jiangsu 225009, ChinaDepartment of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078, USACollege of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan 450002, ChinaMacrophages are crucial members of the mononuclear phagocyte system essential to protect the host from invading pathogens and are central to the inflammatory response with their ability to acquire specialized phenotypes of inflammatory (M1) and anti-inflammatory (M2) and to produce a pool of inflammatory mediators. Equipped with a broad range of receptors, such as Toll-like receptor 4 (TLR4), CD14, and Fc gamma receptors (FcγRs), macrophages can efficiently recognize and phagocytize invading pathogens and secrete cytokines by triggering various secondary signaling pathways. Phospholipase C (PLC) is a family of enzymes that hydrolyze phospholipids, the most significant of which is phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2]. Cleavage at the internal phosphate ester generates two second messengers, inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG), both of which mediate in diverse cellular functions including the inflammatory response. Recent studies have shown that some PLC isoforms are involved in multiple stages in TLR4-, CD14-, and FcγRs-mediated activation of nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and interferon regulatory factors (IRFs), all of which are associated with the regulation of the inflammatory response. Therefore, secondary signaling by PLC is implicated in the pathogenesis of numerous inflammatory diseases. This review provides an overview of our current knowledge on how PLC signaling regulates the macrophage-mediated inflammatory response.http://dx.doi.org/10.1155/2018/5201759
spellingShingle Liqian Zhu
Clinton Jones
Gaiping Zhang
The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response
Journal of Immunology Research
title The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response
title_full The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response
title_fullStr The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response
title_full_unstemmed The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response
title_short The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response
title_sort role of phospholipase c signaling in macrophage mediated inflammatory response
url http://dx.doi.org/10.1155/2018/5201759
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