C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats

Background. C-reactive protein (CRP), a biomarker of inflammation, is highly expressed in osteoarthritis- (OA-) related diseases, but its exact role remains unknown. In this study, we evaluated the biological effect of CRP on temporomandibular joint (TMJ) inflammation. Methods. Freund’s complete adj...

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Main Authors: Yao He, Mengjiao Zhou, Zixiang Jian, Lingli Fang, Lan Huang, Jinlin Song
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2022/8613986
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author Yao He
Mengjiao Zhou
Zixiang Jian
Lingli Fang
Lan Huang
Jinlin Song
author_facet Yao He
Mengjiao Zhou
Zixiang Jian
Lingli Fang
Lan Huang
Jinlin Song
author_sort Yao He
collection DOAJ
description Background. C-reactive protein (CRP), a biomarker of inflammation, is highly expressed in osteoarthritis- (OA-) related diseases, but its exact role remains unknown. In this study, we evaluated the biological effect of CRP on temporomandibular joint (TMJ) inflammation. Methods. Freund’s complete adjuvant (CFA) was used to induce TMJ inflammation in CRP-knockout (CRP-/-) and control rats. Degenerative changes in the TMJ were compared to elucidate the role of CRP in TMJ inflammation. In addition, inflammatory cytokines, macrophage activation, and osteoclast differentiation were evaluated by real-time quantitative polymerase chain reaction, immunohistochemistry, and tartrate-resistant phosphatase staining to explore the potential regulatory mechanism. Results. Compared to the control, CFA induced TMJ inflammation, which increased systemic and local CRP expression. Furthermore, CRP-/- rats exhibited less severe inflammatory symptoms. The downregulation of proinflammatory cytokines (interleukin- (IL-) 1β and IL-6) and upregulation of the anti-inflammatory cytokine IL-10 were detected in CRP-/- rats, which also exhibited reduced macrophage activation and osteoclast differentiation. Conclusion. These results indicated that controlling the highly elevated levels of CRP during inflammation could modify the cytokine profile, macrophage activation, and osteoclast differentiation, thus, providing beneficial effects for TMJ-OA prevention and treatment.
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spelling doaj-art-46cd9313b5b14fd19cd20876c8eb5ff02025-02-03T06:05:31ZengWileyJournal of Immunology Research2314-71562022-01-01202210.1155/2022/8613986C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in RatsYao He0Mengjiao Zhou1Zixiang Jian2Lingli Fang3Lan Huang4Jinlin Song5Department of OrthodonticsDepartment of OrthodonticsDepartment of OrthodonticsDepartment of OrthodonticsDepartment of OrthodonticsDepartment of OrthodonticsBackground. C-reactive protein (CRP), a biomarker of inflammation, is highly expressed in osteoarthritis- (OA-) related diseases, but its exact role remains unknown. In this study, we evaluated the biological effect of CRP on temporomandibular joint (TMJ) inflammation. Methods. Freund’s complete adjuvant (CFA) was used to induce TMJ inflammation in CRP-knockout (CRP-/-) and control rats. Degenerative changes in the TMJ were compared to elucidate the role of CRP in TMJ inflammation. In addition, inflammatory cytokines, macrophage activation, and osteoclast differentiation were evaluated by real-time quantitative polymerase chain reaction, immunohistochemistry, and tartrate-resistant phosphatase staining to explore the potential regulatory mechanism. Results. Compared to the control, CFA induced TMJ inflammation, which increased systemic and local CRP expression. Furthermore, CRP-/- rats exhibited less severe inflammatory symptoms. The downregulation of proinflammatory cytokines (interleukin- (IL-) 1β and IL-6) and upregulation of the anti-inflammatory cytokine IL-10 were detected in CRP-/- rats, which also exhibited reduced macrophage activation and osteoclast differentiation. Conclusion. These results indicated that controlling the highly elevated levels of CRP during inflammation could modify the cytokine profile, macrophage activation, and osteoclast differentiation, thus, providing beneficial effects for TMJ-OA prevention and treatment.http://dx.doi.org/10.1155/2022/8613986
spellingShingle Yao He
Mengjiao Zhou
Zixiang Jian
Lingli Fang
Lan Huang
Jinlin Song
C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats
Journal of Immunology Research
title C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats
title_full C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats
title_fullStr C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats
title_full_unstemmed C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats
title_short C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats
title_sort c reactive protein knockout attenuates temporomandibular joint inflammation in rats
url http://dx.doi.org/10.1155/2022/8613986
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AT zixiangjian creactiveproteinknockoutattenuatestemporomandibularjointinflammationinrats
AT linglifang creactiveproteinknockoutattenuatestemporomandibularjointinflammationinrats
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