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A Dual Role for P2X7 Receptor during Porphyromonas gingivalis Infection.

E S Ramos-Junior1, A C Morandini1, C L C Almeida-da-Silva1

  • 1Programa de Imunobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

Journal of Dental Research
|July 9, 2015
PubMed
Summary

Porphyromonas gingivalis subverts inflammasome activation. The P2X7 receptor is crucial for interleukin-1 beta (IL-1β) processing and secretion in macrophages, impacting periodontitis pathogenesis.

Keywords:
ATPIL-1βcytokinesinflammasomemacrophageperiodontitis

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Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Purinergic signaling influences inflammasome activation and inflammatory cytokine release.
  • Porphyromonas gingivalis, linked to periodontitis, can evade immune responses by inhibiting NLRP3 inflammasome activation.
  • Previous work indicated P. gingivalis fimbriae dampen extracellular ATP (eATP)-induced IL-1β secretion via the P2X7 receptor.

Purpose of the Study:

  • To investigate the role of the P2X7 receptor in eATP-induced IL-1β processing and secretion in P. gingivalis-infected macrophages.
  • To elucidate the involvement of NLRP3 inflammasome components in this process.
  • To assess the in vivo relevance and therapeutic potential of targeting the P2X7/NLRP3 pathway in periodontitis.

Main Methods:

  • In vitro studies using P. gingivalis-infected macrophages to assess IL-1β secretion, caspase 1 activation, and pro-IL-1β cleavage.
  • Utilizing P2X7 receptor and NLRP3 inflammasome component knockout models (in vitro and in vivo).
  • Analysis of P2X7 receptor expression and cytokine profiles (IFN-γ, IL-17) in a P. gingivalis oral infection mouse model and human chronic periodontitis tissues.

Main Results:

  • NLRP3 inflammasome components (NLRP3, ASC, caspase 1) were necessary for eATP-induced IL-1β secretion and caspase 1 activation, independent of P. gingivalis fimbriae.
  • Intracellular pro-IL-1β processing occurred independently of NLRP3, ASC, or caspase 1.
  • The P2X7 receptor played a dual role, essential for both eATP-induced IL-1β secretion and intracellular pro-IL-1β processing.
  • P2X7 receptor expression was upregulated in vivo during P. gingivalis infection, and P2rx7(-/-) mice showed reduced IFN-γ and IL-17.
  • P2X7 receptor and NLRP3 transcription were modulated in human chronic periodontitis.

Conclusions:

  • The P2X7 receptor is critical for both the processing and secretion of IL-1β in P. gingivalis-infected macrophages.
  • The P2X7 receptor plays a significant role in the immunopathogenesis of periodontitis.
  • Targeting the P2X7/NLRP3 pathway presents a potential therapeutic strategy for periodontitis.