Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues.

Tytuł:: Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues.
Autorzy:: Li Y; Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.; Department of Periodontology, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Wang X; Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Wang S; Department of Periodontology, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Zhu C; Department of Periodontology, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Guo J; Department of Periodontology, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Li K; Core Research Laboratory, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
Li A; Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.; Department of Periodontology, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Źródło:: Cell proliferation [Cell Prolif] 2020 Oct; Vol. 53 (10), pp. e12886. Date of Electronic Publication: 2020 Aug 14.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: [Oxford, England] : Published for the Cell Kinetics Society, the European Study Group for Cell Proliferation, and the International Cell Cycle Society by Blackwell Scientific Publications, 1991-
MeSH Terms:: Complement C3/*metabolism
Diabetes Mellitus, Type 2/*pathology
Macrophages/*immunology
Periodontitis/*diagnosis
Adult ; Alveolar Process/diagnostic imaging ; Alveolar Process/pathology ; Alveolar Process/physiology ; Animals ; Bone Density ; Complement C3/analysis ; Complement C3/genetics ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetes Mellitus, Type 2/complications ; Female ; Gingival Crevicular Fluid/metabolism ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Macrophage Activation ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Periodontitis/etiology ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
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Grant Information:: xtr012019007 Innovation team project of Xi'an Jiaotong University; 81701037 National Natural Science Foundation of China; 81901019 National Natural Science Foundation of China
Substance Nomenclature:: 0 (Complement C3)
0 (Interleukin-6)
0 (Tumor Necrosis Factor-alpha)
Entry Date(s):: Date Created: 20200815 Date Completed: 20201029 Latest Revision: 20231112
Update Code:: 20240105
PubMed Central ID:: PMC7574872
DOI:: 10.1111/cpr.12886
PMID:: 32794619
: Czasopismo naukowe

Pełny tekst

Objectives: Diabetes aggravates the risk and severity of periodontitis, but the specific mechanism remains confused. Complement 3 (C3) is closely related to complications of type 2 diabetes (T2DM). In the present study, we concentrated on whether C3 mediates the development of periodontitis in T2DM.
Materials and Methods: Levels of C3 in blood and gingival crevicular fluid (GCF) of patients were measured first. A C3-knockout diabetic mouse model was established, real-time PCR, Western blotting and histological investigation were performed to evaluate the progress of periodontitis. Microcomputed tomography (micro-CT) and TRAP staining were performed to detect alveolar bone resorption. Immunofluorescence was performed to detect polarization of macrophages.
Results: Our data showed that C3 levels were elevated in the blood and GCF of T2DM patients compared with non-diabetic individuals. Increased C3 was closely related to the upregulation of inflammatory cytokines including interleukin (IL)-1, IL-6 and tumour necrosis factor-alpha (TNF-α), as well as the decline of the bone volume density (BMD) and bone volume over total volume (BV/TV) of the alveolar bones in diabetic mice. The deletion of C3 inhibited inflammatory cytokines and rescued the decreased BMD and BV/TV of the alveolar bones. C3-mediated polarization of macrophages was responsible for the damage.
Conclusion: T2DM-related upregulation of C3 contributes to the development of periodontitis by promoting macrophages M1 polarization and inhibiting M2 polarization, triggering a pro-inflammatory effect on periodontal tissues.
(© 2020 The Authors. Cell Proliferation published by John Wiley & Sons Ltd.)

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