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Updated: May 5, 2026
Isolation, Processing and Analysis of Murine Gingival Cells
Published on: July 2, 2013
Inflammatory Cytokine Changes in Herpes Simplex Virus Infected Periodontium: An In Vitro Proteomic Study
Yu Zhang1, Ka-Lam Lo1, Chun-Mei Wang2
1Department of Preventive Dentistry, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai, People's Republic of China.
This study identified herpes simplex virus (HSV) biomarkers in periodontitis patients. Toll-like receptor 2 (TLR2) was upregulated, indicating a host antiviral defense against HSV-1 in periodontal tissues.
Area of Science:
- Oral microbiology
- Virology
- Immunology
Background:
- Periodontitis is a leading cause of tooth loss globally.
- Herpes simplex virus (HSV) infection is implicated in periodontal disease pathogenesis.
Purpose of the Study:
- To identify biomarkers related to herpes simplex virus (HSV) in periodontitis patients.
- To analyze the host's antiviral defense mechanisms in periodontal tissues during HSV-1 infection.
Main Methods:
- Proteomic analysis of human gingival fibroblasts (HGFs) using DIA-based liquid chromatography-tandem mass spectrometry.
- Investigation of HSV-1 infection at early (12h) and late (72h) stages.
Main Results:
- Identified 890 differentially expressed proteins.
- Early stage: Upregulation of interferon (IFN) regulatory factor 7, IFN-stimulated genes 15, interleukin 6 (IL6), toll-like receptor 2 (TLR2), and IFN-induced protein (IFI); downregulation of matrix metalloproteinase 2 (MMP2).
- Late stage: Upregulation of IFIs, IL1, and MMP3; downregulation of complement proteins. Activation of pathways including TLR signaling.
Conclusions:
- Identified HGF proteins associated with periodontitis following HSV-1 infection.
- TLR2 may serve as a biomarker for the host's antiviral response to HSV-1 in the periodontium.
- Provides a framework for understanding anti-HSV-1 defense in periodontal tissues.
