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New insights into acne pathogenesis: propionibacterium acnes activates the inflammasome

Emmanuel Contassot1, Lars E French1

  • 1Dermatology Department, University Hospital of Zürich, Zürich, Switzerland.

The Journal of Investigative Dermatology
|January 16, 2014
PubMed

Insights

Propionibacterium acnes (P. acnes) triggers significant inflammation in acne vulgaris by activating the NLRP3 inflammasome and increasing IL-1β secretion. Targeting IL-1β or NLRP3 may offer new acne treatment options.

Area of Science:

  • Dermatology
  • Immunology
  • Microbiology

Background:

  • The role of Propionibacterium acnes (P. acnes) in acne vulgaris pathogenesis is debated.
  • Inflammation is a key feature of acne vulgaris.

Purpose of the Study:

  • To investigate the mechanism by which P. acnes induces inflammation.
  • To determine the role of the NLRP3 inflammasome and IL-1β in P. acnes-mediated inflammation.

Main Methods:

  • Monocytic cells were stimulated with P. acnes.
  • Activation of the NLRP3 inflammasome and IL-1β secretion were measured.
  • In vivo studies examined P. acnes and macrophage interactions in skin.

Main Results:

  • P. acnes induced significant IL-1β secretion in monocytic cells.
  • This secretion was dependent on the activation of the NLRP3 inflammasome.
  • In vivo, P. acnes and macrophages in the dermis led to local IL-1β release and exacerbated inflammation.

Conclusions:

  • P. acnes activates the NLRP3 inflammasome, leading to IL-1β production and inflammation in acne.
  • Targeting IL-1β or the NLRP3 inflammasome presents potential therapeutic strategies for acne vulgaris.

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