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miR-155 promotes macrophage pyroptosis induced by Porphyromonas gingivalis through regulating the NLRP3 inflammasome

Chen Li1, Wanting Yin1,2, Ning Yu3

  • 1Department of Periodontics, School of Stomatology, China Medical University, Shenyang, China.

Oral Diseases
|September 19, 2019
PubMed
Abstract

Insights

Porphyromonas gingivalis infection triggers pyroptosis in macrophages. This process involves miR-155, which regulates the NLRP3 inflammasome, offering insights into early infection mechanisms.

Area of Science:

  • Cellular Biology
  • Immunology
  • Microbiology

Background:

  • Pyroptosis is a programmed cell death pathway crucial in immunity.
  • Porphyromonas gingivalis is a key pathogen in periodontitis, known to interact with host immune cells.

Purpose of the Study:

  • To detect pyroptosis in macrophages stimulated by Porphyromonas gingivalis.
  • To elucidate the mechanism of P. gingivalis-induced pyroptosis, focusing on the role of miR-155 and the NLRP3 inflammasome.

Main Methods:

  • Human monocyte cell line U937 stimulated with P. gingivalis.
  • Flow cytometry to detect pyroptosis.
  • Real-time PCR for miR-155 expression.
  • Western blotting for key pyroptosis-related proteins (GSDMD, Caspases, ASC, NLRP3, SOCS1).
  • ELISA for IL-1β and IL-18.

Main Results:

  • P. gingivalis stimulation increased pyroptosis and miR-155 expression in macrophages.
  • Silencing miR-155 reduced pyroptosis rates.
  • Increased levels of pyroptosis markers (GSDMD-NT, Caspase-1/11, NLRP3, IL-1β, IL-18) and decreased SOCS1 were observed.
  • miR-155 inhibition partially reversed these changes, except for ASC expression.

Conclusions:

  • Porphyromonas gingivalis promotes pyroptosis in macrophages during early infection stages.
  • miR-155 plays a significant role in this process by regulating the NLRP3 inflammasome pathway.
Keywords:
Porphyromonas gingivalisNLRP3macrophagesmiR-155pyroptosis

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