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Propionibacterium acnes-induced iNOS and COX-2 protein expression via ROS-dependent NF-κB and AP-1 activation in

Hsiou-Hsin Tsai1, Woan-Rouh Lee, Pai-Hua Wang

  • 1Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.

Journal of Dermatological Science
|November 27, 2012
PubMed
Abstract

Insights

Propionibacterium acnes infection increases reactive oxygen species (ROS) and inflammatory mediators like nitric oxide (NO) and prostaglandin E2 (PGE2) in macrophages. Hispolon effectively inhibits these P. acnes-induced inflammatory responses.

Area of Science:

  • Immunology
  • Microbiology
  • Dermatology

Background:

  • Propionibacterium acnes (P. acnes) is implicated in inflammatory lesion development.
  • The bacterium's effect on inducible nitric oxide synthase (iNOS)/nitric oxide (NO) and cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) in macrophages remains uninvestigated.

Purpose of the Study:

  • To determine reactive oxygen species (ROS), iNOS/NO, and COX-2/PGE2 production by macrophages after P. acnes infection.
  • To elucidate the mechanism of P. acnes-stimulated iNOS and COX-2 expression and subsequent NO and PGE2 production in RAW264.7 macrophages.

Main Methods:

  • In vitro cell culture system using RAW264.7, J774A.1, and peritoneal macrophages.
  • Analysis of iNOS/NO, COX-2/PGE2, ROS production, and ERK/JNK, AP-1/NF-κB activation via Western blotting, flow cytometry, and luciferase assays.
  • Pharmacological inhibition using ROS scavenger (NAC), NADPH oxidase inhibitor (DPI), and MAPK inhibitors (U0126, SP600125).

Main Results:

  • P. acnes increased iNOS/NO and COX-2/PGE2 expression in a multiplicity of infection (MOI)-dependent manner.
  • Increased ROS production, ERK/JNK phosphorylation, and AP-1/NF-κB activation were observed in P. acnes-induced macrophages.
  • Hispolon significantly inhibited P. acnes-induced iNOS/NO and COX-2/PGE2 production, highlighting the role of its C5-OH group.

Conclusions:

  • ROS-dependent activation of ERK, JNK, NF-κB, and AP-1 pathways mediates P. acnes-induced iNOS/NO and COX-2/PGE2 production in macrophages.
  • Hispolon demonstrates potential for treating early-phase inflammation caused by P. acnes by blocking iNOS/NO and COX-2/PGE2 production.

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