Triclosan inhibition of acute and chronic inflammatory gene pathways

J Clin Periodontol. 2010 May;37(5):412-8. doi: 10.1111/j.1600-051X.2010.01548.x.


Aim: We sought to determine whether triclosan (2,4,4'-trichloro-2'-hydroxydiphenylether), an extensively used anti-plaque agent with broad-spectrum anti-microbial activity, with reported anti-inflammatory effects via inhibition of prostaglandin E2 and interleukin 1 (IL-1)beta, could also more broadly suppress multiple inflammatory gene pathways responsible for the pathogenesis of gingivitis and periodontitis.

Materials and methods: As an exploratory study, the effects of triclosan on the inflammatory gene expression profile were assessed ex vivo using peripheral whole blood samples from eight periodontally healthy donors. Ten-millilitres whole blood aliquots were incubated 2 h with 0.3 microg/ml Escherichia coli lipopolysaccharide (LPS) with or without 0.5 microg/ml triclosan. Affymetrix microarray gene expression profiles from isolated leucocytes and pathway-specific quantitative polymerase chain reaction arrays were used to investigate changes in expression of target cytokines and cell signalling molecules.

Results: Ex vivo human whole blood assays indicated that triclosan significantly down-regulated the LPS-stimulated expression of Toll-like receptor signalling molecules and other multiple inflammatory molecules including IL-1 and IL-6 and the dampening of signals that activate the T-helper type 1 acquired immune response via suppression of CD70 with concomitant up-regulation of growth factors related to bone morphogenetic protein (BMP)2 and BMP6 synthesis.

Conclusions: Anti-inflammatory effects were found in this exploratory survey, including suppression of microbial-pathogen recognition pathway molecules and the suppression of acute and chronic mediators of inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adult
  • Anti-Inflammatory Agents / pharmacology*
  • Bone Morphogenetic Protein 2 / biosynthesis
  • Bone Morphogenetic Protein 2 / genetics
  • Bone Morphogenetic Protein 6 / biosynthesis
  • Bone Morphogenetic Protein 6 / genetics
  • CD27 Ligand / antagonists & inhibitors
  • Chronic Disease
  • Female
  • Gene Expression Profiling*
  • Host-Pathogen Interactions / drug effects
  • Humans
  • Inflammation / genetics*
  • Inflammation Mediators / antagonists & inhibitors*
  • Interleukin-1 / antagonists & inhibitors
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / genetics
  • Interleukin-6 / antagonists & inhibitors
  • Interleukin-6 / biosynthesis
  • Interleukin-6 / genetics
  • Lipopolysaccharides / pharmacology
  • Male
  • Oligonucleotide Array Sequence Analysis
  • Signal Transduction / drug effects
  • Th1 Cells / immunology
  • Toll-Like Receptors / antagonists & inhibitors
  • Toll-Like Receptors / biosynthesis
  • Toll-Like Receptors / genetics*
  • Triclosan / pharmacology*
  • Young Adult


  • Anti-Inflammatory Agents
  • Bone Morphogenetic Protein 2
  • Bone Morphogenetic Protein 6
  • CD27 Ligand
  • Inflammation Mediators
  • Interleukin-1
  • Interleukin-6
  • Lipopolysaccharides
  • Toll-Like Receptors
  • Triclosan