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Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3

Yazdani B Shaik-Dasthagirisaheb1, Nasi Huang, Frank C Gibson

  • 1Section of Infectious Diseases, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.

Innate Immunity
|June 28, 2013
PubMed

Insights

Interferon regulatory factor 3 (IRF3) plays a key role in the inflammatory response to Porphyromonas gingivalis, a bacterium linked to periodontal disease. This study reveals IRF3

Area of Science:

  • Immunology
  • Microbiology
  • Periodontology

Background:

  • Periodontal disease (PD) involves chronic inflammation driven by innate immune activation.
  • Porphyromonas gingivalis, a key pathogen in PD, triggers TLR-mediated signaling pathways.
  • The role of Interferon regulatory factor 3 (IRF3) in the host response to P. gingivalis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of IRF3 in the inflammatory response of macrophages to Porphyromonas gingivalis.
  • To elucidate the signaling pathways involved in IRF3 activation and its downstream effects.

Main Methods:

  • Utilized bone marrow-derived macrophages (MØ) from wild-type (WT) and knockout mice (IRF3-/-, TRIF-/-, TLR4-/-, IRF7-/-).
  • Stimulated MØ with P. gingivalis and assessed inflammatory cytokine production (TNF-α, IL-6, RANTES).
  • Analyzed IRF3 activation and nuclear translocation via Western blotting and immunofluorescence.

Main Results:

  • P. gingivalis induced IRF3 activation and nuclear translocation in WT MØ.
  • MØ from IRF3-/-, TRIF-/-, and TLR4-/- mice exhibited reduced TNF-α production upon P. gingivalis challenge compared to WT.
  • IRF3 was essential for the full expression of IL-6 and RANTES in response to P. gingivalis.
  • IRF3 played a significant role, while IRF7 played a modest role in P. gingivalis-induced TNF-α production.

Conclusions:

  • IRF3 is a critical mediator of the inflammatory response by macrophages to the periodontal pathogen P. gingivalis.
  • The TRIF-dependent pathway and TLR4 are involved in IRF3-mediated responses to P. gingivalis.
  • These findings highlight IRF3 as a potential therapeutic target for managing periodontal inflammation.
Keywords:
IRF3Porphyromonas gingivalischemokinecytokinemacrophage

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