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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Format: | Article |
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BMC
2019-10-01
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Series: | Molecular Brain |
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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. |
first_indexed | 2024-12-13T15:54:51Z |
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id | doaj.art-c7f471f51005481b8e5a38bc2fe92b48 |
institution | Directory Open Access Journal |
issn | 1756-6606 |
language | English |
last_indexed | 2024-12-13T15:54:51Z |
publishDate | 2019-10-01 |
publisher | BMC |
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series | Molecular Brain |
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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