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Updated: Dec 30, 2025
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
EMMPRIN-CypA contributes to the inflammatory processes in human periodontitis through infiltrating CD68+ inflammatory
Lande Xue1, Linwang Su2, Jianli Xie1
1Department of Endodontics, Jinan Stomatological Hospital Jinan, Shandong, China.
Abstract:
Extracellular matrix metalloproteinase inducer (EMMPRIN) and its ligand cyclophilin A (CypA) levels increase in human inflammatory diseases, but EMMPRIN-CypA interactions and cell types expressing EMMPRIN and CypA in the pathogenesis of periodontitis are uncertain. Immunohistochemistry, immunofluorescence and western blotting revealed the level of EMMPRIN, CypA, and CD68 in human periodontitis. Double labelled immunofluorescence colocalized the expression of CD68 and CypA, and CD68 and EMMPRIN. Further investigation of EMMPRIN-CypA interactions and CD68+ infiltrating cells was applied using mouse monocyte cell line RAW264.7 in vitro. A higher level of EMMPRIN and CypA staining was detected in human periodontitis, compared with healthy gingiva. Many inflammatory cells, including CD68+ cells, infiltrated gingival tissues of human periodontitis. Both EMMPRIN and CypA could be localized in the CD68+ infiltrating cells. CypA could induce NF-κB activation by increasing expression of NFκB p-p65 in the nucleus of mouse monocytic cells RAW264.7 in vitro. EMMPRIN-CypA may contribute to the inflammatory processes in human periodontitis through infiltrating CD68+ inflammatory cells.
Insights
Extracellular matrix metalloproteinase inducer (EMMPRIN) and cyclophilin A (CypA) are elevated in periodontitis. These molecules interact within CD68-positive inflammatory cells, suggesting a role in periodontitis pathogenesis.
Area of Science:
- Oral Biology
- Immunology
- Biochemistry
Background:
- Extracellular matrix metalloproteinase inducer (EMMPRIN) and cyclophilin A (CypA) are implicated in inflammatory diseases.
- The specific roles of EMMPRIN-CypA interactions and their cellular sources in periodontitis remain unclear.
Purpose of the Study:
- To investigate EMMPRIN and CypA expression and their interactions in human periodontitis.
- To identify the cell types involved in EMMPRIN and CypA expression within periodontitis lesions.
- To explore the functional consequences of EMMPRIN-CypA interactions in vitro.
Main Methods:
- Immunohistochemistry, immunofluorescence, and Western blotting were used to detect EMMPRIN, CypA, and CD68 in human gingival tissues.
- Double immunofluorescence confirmed co-localization of EMMPRIN and CypA with CD68-positive cells.
- In vitro studies using the RAW264.7 cell line assessed NF-κB activation.
Main Results:
- Elevated levels of EMMPRIN and CypA were observed in periodontitis tissues compared to healthy controls.
- EMMPRIN and CypA were localized within CD68-positive infiltrating inflammatory cells in periodontitis.
- CypA induced NF-κB activation in mouse monocytic cells, indicated by increased nuclear NFκB p-p65.
Conclusions:
- EMMPRIN and CypA are upregulated in human periodontitis.
- The EMMPRIN-CypA complex is present in CD68-positive inflammatory cells, suggesting their involvement in the disease.
- EMMPRIN-CypA interactions may drive inflammatory processes in periodontitis via these infiltrating cells.
