Hyperglucose Contributes to Periodontitis: Involvement of the NLRP3 Pathway by Engaging the Innate Immunity of Oral Gingival Epithelium

Background: The NLRP3 inflammasome is essentially a family of intracellular innate immune sensors that can respond to bacterial challenge and initiate early host immunity responses. However, the involvement and possible molecular mechanism of the NLRP3 pathway in the context of chronic periodontitis...

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Bibliographic Details
Published in:Journal of periodontology (1970) 2015-02, Vol.86 (2), p.327-335
Main Authors: Huang, Xin, Yang, Xi, Ni, Jia, Xie, Baoyi, Liu, Yeungyeung, Xuan, Dongying, Zhang, Jincai
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Aged, 80 and over
Carrier Proteins - analysis
Carrier Proteins - antagonists & inhibitors
Carrier Proteins - immunology
Caspase 1 - analysis
Caspase 1 - immunology
Cells, Cultured
Chronic periodontitis
Chronic Periodontitis - immunology
Dentistry
diabetes mellitus, type 2
Diabetes Mellitus, Type 2 - immunology
Epithelial Cells - drug effects
Epithelial Cells - immunology
Female
Gingiva - cytology
Gingiva - immunology
Glucose - immunology
Humans
Hyperglycemia - complications
immunity, innate
Immunity, Innate - immunology
Interleukin-1beta - analysis
Interleukin-1beta - immunology
Lipopolysaccharides - immunology
Male
Middle Aged
NLR family, pyrin domain containing 3 protein, human
NLR Family, Pyrin Domain-Containing 3 Protein
NLRP3 protein, human
Potassium - pharmacology
Signal Transduction - immunology
Young Adult
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Summary:Background: The NLRP3 inflammasome is essentially a family of intracellular innate immune sensors that can respond to bacterial challenge and initiate early host immunity responses. However, the involvement and possible molecular mechanism of the NLRP3 pathway in the context of chronic periodontitis (CP) and diabetes mellitus have yet to be fully elucidated. Methods: Gingival tissues were collected from patients with CP and/or type 2 diabetes mellitus (T2DM), and the expression of NLRP3 and interleukin (IL)‐1β was analyzed by immunohistochemistry. To explore the possible molecular mechanism, human gingival epithelial cells (HGECs) were established in vitro and challenged with lipopolysaccharide (LPS) and/or high glucose. High extracellular K+ was applied as an inhibitor of NLRP3. The NLRP3 pathway was analyzed by immunocytochemistry and quantitative polymerase chain reaction. Results: Compared with control individuals, NLRP3 and IL‐1β were significantly upregulated in oral gingival epithelium of patients with CP and/or T2DM (P
ISSN:0022-3492
1943-3670
DOI:10.1902/jop.2014.140403