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Propionibacterium acnes stimulates pro-matrix metalloproteinase-2 expression through tumor necrosis factor-alpha in

Jee-Young Choi1, Mei Shan Piao, Jee-Bum Lee

  • 1Department of Dermatology, Chonnam National University Medical School, Gwangju, Korea.

The Journal of Investigative Dermatology
|December 1, 2007
PubMed

Insights

Propionibacterium acnes stimulates dermal fibroblasts to produce pro-matrix metalloproteinase-2, contributing to acne tissue remodeling. This process involves tumor necrosis factor-alpha and the NF-kappaB pathway, and can be inhibited by doxycycline.

Area of Science:

  • Dermatology
  • Microbiology
  • Molecular Biology

Background:

  • Propionibacterium acnes (P. acnes) is a skin commensal involved in acne inflammation.
  • The role of P. acnes in dermal tissue remodeling during acne is unknown.

Purpose of the Study:

  • Investigate if P. acnes induces matrix metalloproteinase (MMP) in human dermal fibroblasts (hDF).
  • Elucidate the molecular pathways involved in P. acnes-induced MMP expression.

Main Methods:

  • Treated hDF with P. acnes and measured proMMP-2, proMMP-9, and TNF-alpha mRNA/protein expression.
  • Investigated the role of the NF-kappaB pathway.
  • Assessed the effect of doxycycline on P. acnes-induced proMMP-2 expression.

Main Results:

  • P. acnes increased proMMP-2 mRNA/protein expression in hDF, but not proMMP-9.
  • P. acnes induced TNF-alpha expression, which mediated proMMP-2 upregulation via the NF-kappaB pathway.
  • Doxycycline inhibited P. acnes- and TNF-alpha-induced proMMP-2 expression.

Conclusions:

  • P. acnes stimulates hDF to produce TNF-alpha, leading to proMMP-2 expression through the NF-kappaB pathway.
  • P. acnes-induced proMMP-2 secretion may contribute to acne-related tissue remodeling.
  • Doxycycline shows potential in mitigating P. acnes-driven matrix remodeling in acne.

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