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Neutrophil extracellular traps induced by Porphyromonas gingivalis lipopolysaccharide modulate inflammatory responses

Jia-Lu Chen1, Yue Tong1, Qin Zhu1

  • 1Department of Periodontology, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China,; Jiangsu Province Key Laboratory of Oral Diseases, Nanjing, China,; Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing, China.

Archives of Oral Biology
|June 9, 2022
PubMed
Abstract

Insights

Porphyromonas gingivalis lipopolysaccharide (LPS) triggers neutrophil extracellular traps (NETs) formation, enhancing bacterial killing. This process involves a specific signaling pathway crucial for eliminating P. gingivalis.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Neutrophil extracellular traps (NETs) are crucial in host defense against bacterial pathogens.
  • Porphyromonas gingivalis (P. gingivalis) is a key bacterium implicated in periodontal disease.
  • The role of P. gingivalis lipopolysaccharide (LPS) in NET formation requires further elucidation.

Purpose of the Study:

  • To investigate the impact of P. gingivalis LPS on NET formation.
  • To elucidate the underlying molecular mechanisms involved in LPS-induced NETosis.

Main Methods:

  • NET formation was induced by P. gingivalis LPS and visualized using fluorescence microscopy.
  • Bactericidal activity of NETs against P. gingivalis was assessed.
  • Intracellular calcium (Ca2+) levels, signaling pathway components (p-TPL2, p-MEK1/2, p-ERK1/2), ion channels (ORAI1, ORAI2), and PAD4 expression were analyzed via flow cytometry and Western blot.
  • Neutrophil elastase activity in NETs was measured after co-culture with macrophages.

Main Results:

  • P. gingivalis LPS significantly induced NET formation and increased extracellular DNA release, enhancing neutrophil bactericidal activity.
  • Treatment with P. gingivalis LPS elevated intracellular Ca2+ levels and upregulated key signaling molecules including p-TPL2, p-MEK1/2, p-ERK1/2, ORAI1, ORAI2, and PAD4.
  • Inhibition of Ca2+ or knockdown of PAD4 reduced extracellular DNA release, confirming their roles in NET formation.
  • NETs demonstrated clearance capacity, indicated by decreased neutrophil elastase activity after co-culture with macrophages.

Conclusions:

  • P. gingivalis LPS induces NET formation through a signaling cascade involving Ca2+, TPL2, MEK, ERK, and PAD4.
  • This LPS-induced NETosis mechanism contributes to the elimination of P. gingivalis bacteria.
Keywords:
Ca(2+)LipopolysaccharideNeutrophil extracellular trapsPorphyromonas gingivalis

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