期刊
MOLECULAR IMMUNOLOGY
卷 103, 期 -, 页码 209-219出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2018.10.001
关键词
Nlrp3 inflammasome; Reactive oxygen species; Porphyromonas gingivalis; Lipopolysaccharides; Cell migration inhibition
资金
- National Natural Science Foundation of China [81603587, 81603668]
- National Key Research and Development Program of China [2017YFC1700400]
- Guangdong Natural Science Funds for Distinguished Young Scholar [2018B030306027]
- Science and Technology Development Plan of Guangdong Province [2017A020211016]
- Youth Medical Talent Fund of Guangzhou University of Chinese Medicine [QNYC20170105]
- Science & Technology Award for Young-aged Talents of China Association of Traditional Chinese Medicine [CACM-2017-QNRC2-C12]
- Project of Guangzhou University of Chinese Medcine [A1-AFD018171Z11020]
- Fundamental Research Funds for the Central Universities [11616334]
Inflammasomes serve as an intracellular machinery to initiate inflammatory response to various danger signals. However, the chronic periodontitis pathological relevance of this inflammasome activation, particularly in periodontal ligament fibroblasts, remains largely unknown. The present study demonstrated that Nlrp3 inflammasome components abundantly expressed in cultured mouse periodontal ligament fibroblasts (mPDLFs). In addition, our data demonstrated that P.g-LPS (Porphyromonas gingivalis Lipopolysaccharide), a major injurious factor during chronic periodontitis, could induce the mPDLFs migration dysfunction and the inhibition of Nlrp3 inflammasome by Isoliquiritigenin (ISO) markedly recovered the migration dysfunction in mPDLFs. And Nlrp3 inflammasome components could be aggregated to form an inflammasome complex on stimulation of P.g-LPS, as shown by fluorescence confocal microscopy. Correspondingly, P.g-LPS induced Nlrp3 inflammasome activation, caspase-1 activation, IL-1 beta and HMGB1 release, which were blocked by Nlrp3 inflammasome inhibitor (ISO). Interestingly, reactive oxygen species, TXNIP protein and TXNIP binding to Nlrp3 were markedly increased in mPDLFs with P.g-LPS. Furthermore, ROS generation inhibitor (Apocynin; APO) significantly reduced Nlrp3 inflammasome formation and IL-1 beta production in mPDLFs with P.g-LPS. And APO attenuated P.g-LPS-induced TXNIP protein expression and mPDLFs injury. In conclusion, our results demonstrate that ROS/TXNIP/Nlrp3 Inflammasome pathway is a key initiating mechanism necessary for P.g-LPS-induced subsequent mPDLFs inflammatory response leading to chronic periodontitis.
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