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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.
Objective:
Periodontitis is the primary cause of tooth loss worldwide. This study aimed to identify herpes simplex virus (HSV) related biomarkers in periodontitis patients.
Methods:
The present study used DIA-based liquid chromatography-tandem mass spectrometry to analyze the proteome of human gingival fibroblasts (HGFs) from one healthy donor across early and late stages (12-72 h) of HSV-1 infection.
Results:
The study identified 890 differentially expressed proteins. At the early infection stage, there was a notable upregulation of proteins including interferon (IFN) regulatory factor 7, IFN-stimulated genes 15, interleukin 6 (IL6), toll-like receptor 2 (TLR2), and IFN-induced protein (IFI), alongside a downregulation of matrix metalloproteinase 2 (MMP2). We observed the activation of pathways, including the complement and coagulation cascades, lysosome, nucleotide-binding oligomerization domain-like receptors, retinoic acid-inducible gene I-like receptors, and TLR signaling pathways. Conversely, at the late stage, IFIs, IL1, and MMP3 were significantly upregulated, while complement proteins were downregulated. Biomarkers such as TLR2 may underscore the host's antiviral defense response to HSV-1 in the periodontal environment.
Conclusions:
The present study identified several HGF proteins associated with periodontitis following HSV-1 infection, providing an analytical framework for determining the host's anti-viral defense response to antagonize HSV-1 infection in periodontal tissues.
