Activation of toll-like receptor 2 in acne triggers inflammatory cytokine responses

Jenny Kim1, Maria-Teresa Ochoa, Stephan R Krutzik

  • 1Division of Dermatology, University of California, Los Angeles, School of Medicine, Los Angeles, CA 90095, USA.

Insights

Propionibacterium acnes triggers inflammation in acne by activating Toll-like receptor 2 (TLR2). This discovery suggests TLR2 as a potential therapeutic target for acne treatment.

Area of Science:

  • Dermatology
  • Immunology
  • Microbiology

Background:

  • Propionibacterium acnes (P. acnes) contributes to acne pathogenesis.
  • The molecular mechanisms of P. acnes-induced inflammation remain unclear.
  • Microbial agents can trigger cytokine responses through Toll-like receptors (TLRs).

Purpose of the Study:

  • To investigate if Toll-like receptor 2 (TLR2) mediates P. acnes-induced cytokine production in acne.
  • To explore the role of TLR2 in the inflammatory pathways of acne.

Main Methods:

  • Transfection of TLR2 into a nonresponsive cell line to assess NF-kappa B activation.
  • Utilizing peritoneal macrophages from wild-type and knockout mice (TLR6, TLR1, TLR2).
  • Analyzing IL-12 p40 promoter activity and cytokine (IL-12, IL-8) protein production in human monocytes.
  • Examining TLR2 expression in acne lesions using immunohistochemistry.

Main Results:

  • P. acnes induced NF-kappa B activation in cells transfected with TLR2.
  • Macrophages from TLR2 knockout mice did not produce IL-6 in response to P. acnes.
  • P. acnes activated IL-12 p40 promoter activity via TLR2.
  • P. acnes stimulated IL-12 and IL-8 production in human monocytes, inhibited by anti-TLR2 antibodies.
  • TLR2 was found on macrophages within acne lesions.

Conclusions:

  • P. acnes activates inflammatory cytokine responses in acne through TLR2.
  • TLR2 plays a significant role in mediating the inflammatory process of acne.
  • TLR2 represents a potential novel therapeutic target for acne treatment.

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