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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Oral Health 1/2015

The activation of pyrin domain-containing-3 inflammasome depends on lipopolysaccharide from Porphyromonas gingivalis and extracellular adenosine triphosphate in cultured oral epithelial cells

BMC Oral Health > Ausgabe 1/2015
Wei Guo, Peng Wang, Zhonghao Liu, Pishan Yang, Ping Ye
Wichtige Hinweise

Competing interests

All authors declare that they have no competing interests.

Authors’ contributions

WG performed the experimental studies and data analysis, and contributed to the draft of manuscript. PW contributed to data analysis of western blot. ZHL supported WG. and provided oversight for this study. PSY contributed to the revision of manuscript. PY provided oversight for this study and the revision of manuscript. All authors read and approved the final manuscript.



Gingival epithelial cells are the major population of the gingival tissue, acting as the front-line defense against microbial intrusion and regulating the homeostasis of the periodontal tissue in health and disease via NLR family pyrin domain-containing-3 (NLRP3) inflammasome, which recognizes pathogen- and danger-associated molecular patterns (PAMPs and DAMPs). The aim of this study was to determine whether the activation of NLRP3 inflammasome depends on infection with the periodontal pathogen Porphyromonas gingivalis (P. gingivalis), or stimulation with P. gingivalis lipopolysaccharide (LPS), and/or extracellular adenosine triphosphate (ATP).


An oral epithelial cell line was treated with P. gingivalis, P. gingivalis LPS and ATP. The gene and protein expression of NLRP3 inflammasome components were quantified by real time RT-PCR and immunoblots. Production of IL-1β and IL-18 was measured by ELISA.


There was no increase in NLRP3 inflammasome gene expression after P. gingivalis infection unless pre-stimulated by ATP. Obvious increases of NLRP3 inflammasome gene expression was observed after P. gingivalis LPS stimulation, even pre-stimulated by ATP at 2 h.


The findings indicate that the activation of NLRP3 inflammasome does not rely on P. gingivalis infection, unless stimulated by P. gingivalis LPS and/or extracellular ATP, suggesting diverse signaling pathways are involved in the host immune response.
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