The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats

Abstract The Fc gamma receptor I (FcγRI; CD64) is the high-affinity receptor of the immunoglobulin G protein (IgG). It is usually expressed in immune cells and has recently been identified to distribute in the nervous system and play critical roles in various neurological disorders. Presently, the i...

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Main Authors: Yingxia Liang, Zhiyu Zhang, Zhaodong Juan, Rui Zhang, Can Zhang
Format: Article
Language:English
Published: BMC 2019-10-01
Series:Molecular Brain
Subjects:
Online Access:http://link.springer.com/article/10.1186/s13041-019-0499-3
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author Yingxia Liang
Zhiyu Zhang
Zhaodong Juan
Rui Zhang
Can Zhang
author_facet Yingxia Liang
Zhiyu Zhang
Zhaodong Juan
Rui Zhang
Can Zhang
author_sort Yingxia Liang
collection DOAJ
description Abstract The Fc gamma receptor I (FcγRI; CD64) is the high-affinity receptor of the immunoglobulin G protein (IgG). It is usually expressed in immune cells and has recently been identified to distribute in the nervous system and play critical roles in various neurological disorders. Presently, the impacts of FcγRI in neuropathic pain was largely unknown. Here, we aimed to investigate the impacts of FcγRI in neuropathic pain through pain-related neurobehavioral studies and underlying mechanisms by biochemical methods in animal and cell models. Specifically, we first utilized the chronic constriction injury (CCI) rat model that displayed neuropathic pain related symptoms and signs, including thermal hyperalgesia and mechanical allodynia. These neurobehavioral defects were significantly attenuated by the anti-FcγRI antibody, which was associated with reduced levels of neuropeptide substance P, C3, and TNF-α. Furthermore, we validated our animal findings using the embryonically neural crest-originated PC12 cell model. We found that stimulation of the IgG immune complex led to increased levels of FcγRI and inflammatory mediators, which were attenuated by the anti-FcγRI antibody in these cells. Collectively, our results from animal and cell-based studies suggest that FcγRI is a critical player for peripheral nerve injury-induced neuropathic pain by mediating pain-related immunological events, which therefore may provide a new therapeutic target for protection against chronic pain.
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spelling doaj.art-c7f471f51005481b8e5a38bc2fe92b482022-12-21T23:39:20ZengBMCMolecular Brain1756-66062019-10-011211410.1186/s13041-019-0499-3The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in ratsYingxia Liang0Zhiyu Zhang1Zhaodong Juan2Rui Zhang3Can Zhang4Department of Anesthesiology, Weifang Medical UniversityDepartment of Trauma Orthopedics, Shouguang People’s HospitalDepartment of Anesthesiology, Weifang Medical UniversityDepartment of Anesthesiology, Weifang Medical UniversityGenetics and Aging Research Unit, McCance Center for Brain Health, Department of Neurology, MassGeneral Institute for Neurodegenerative Diseases (MIND), Massachusetts General Hospital and Harvard Medical SchoolAbstract The Fc gamma receptor I (FcγRI; CD64) is the high-affinity receptor of the immunoglobulin G protein (IgG). It is usually expressed in immune cells and has recently been identified to distribute in the nervous system and play critical roles in various neurological disorders. Presently, the impacts of FcγRI in neuropathic pain was largely unknown. Here, we aimed to investigate the impacts of FcγRI in neuropathic pain through pain-related neurobehavioral studies and underlying mechanisms by biochemical methods in animal and cell models. Specifically, we first utilized the chronic constriction injury (CCI) rat model that displayed neuropathic pain related symptoms and signs, including thermal hyperalgesia and mechanical allodynia. These neurobehavioral defects were significantly attenuated by the anti-FcγRI antibody, which was associated with reduced levels of neuropeptide substance P, C3, and TNF-α. Furthermore, we validated our animal findings using the embryonically neural crest-originated PC12 cell model. We found that stimulation of the IgG immune complex led to increased levels of FcγRI and inflammatory mediators, which were attenuated by the anti-FcγRI antibody in these cells. Collectively, our results from animal and cell-based studies suggest that FcγRI is a critical player for peripheral nerve injury-induced neuropathic pain by mediating pain-related immunological events, which therefore may provide a new therapeutic target for protection against chronic pain.http://link.springer.com/article/10.1186/s13041-019-0499-3Neuropathic painFc gamma receptorAnti-FcγRI antibodySpinal cordPeripheral nerve injuryInflammatory mediators
spellingShingle Yingxia Liang
Zhiyu Zhang
Zhaodong Juan
Rui Zhang
Can Zhang
The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats
Molecular Brain
Neuropathic pain
Fc gamma receptor
Anti-FcγRI antibody
Spinal cord
Peripheral nerve injury
Inflammatory mediators
title The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats
title_full The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats
title_fullStr The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats
title_full_unstemmed The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats
title_short The high-affinity IgG receptor FcγRI modulates peripheral nerve injury-induced neuropathic pain in rats
title_sort high affinity igg receptor fcγri modulates peripheral nerve injury induced neuropathic pain in rats
topic Neuropathic pain
Fc gamma receptor
Anti-FcγRI antibody
Spinal cord
Peripheral nerve injury
Inflammatory mediators
url http://link.springer.com/article/10.1186/s13041-019-0499-3
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