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. 2013 Apr;19(3):296-302.
doi: 10.1111/odi.12001.

Triclosan alters antimicrobial and inflammatory responses of epithelial cells

M A Wallet  1 , N l Calderon, T R Alonso, C S Choe, D l Catalfamo, C J Lalane, K G Neiva, F Panagakos, S M Wallet
Affiliations

Triclosan alters antimicrobial and inflammatory responses of epithelial cells

M A Wallet et al. Oral Dis. 2013 Apr.

Abstract

Periodontal diseases are a class of pathologies wherein oral microbes induce harmful immune responses in a susceptible host. Therefore, an agent that can both reduce microbial burden and lessen pathogenesis of localized inflammation would have beneficial effects in periodontal disease; 2,4,4-trichloro-2-hydroxydiphenyl-ether [triclosan] is currently used in oral care products owing to broad spectrum antimicrobial and anti-inflammatory properties.

Objective: To determine effects of triclosan on the response of oral epithelial cells to stimulation with the inflammatory microbial product lipopolysaccharide (LPS), a ligand for toll-like receptor 4 [TLR4].

Materials/methods: Primary human oral epithelial cells were stimulated with LPS in the presence and/or absence of triclosan after which expression of pro-inflammatory cytokines, β-defensins, micro-RNAs [miRNAs], or TLR-signaling pathway proteins were evaluated.

Results: Here, we demonstrate that triclosan is a potent inhibitor of oral epithelial cell LPS-induced pro-inflammatory responses by inducing miRNA regulation of the TLR-signaling pathway. Triclosan was not a pan-suppresser of oral epithelial cell responses as β-defensin 2 [βD2] and βD3 were upregulated by triclosan following LPS-stimulation.

Conclusions: These data demonstrate both a novel antimicrobial mechanism by which triclosan improves plaque control and an additional anti-inflammatory property, which could have beneficial effects in periodontal disease resolution.

Keywords: chemokines; cytokines; defensins; inflammation; oral epithelial cells; triclosan.

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Conflict of interest statement

Conflicts of Interest

No conflicts of interest are reported by any of the authors.

Figures

Figure 1
Figure 1. Simultaneous treatment with triclosan inhibits LPS-induced inflammatory cytokine secretion by monocytes and fibroblasts but not by oral epithelial cells
(A) THP1, (B) HPLF, and (C) HOK were simultaneously treated with 0.25, 0.50, 0.75 or 1.0ug/ml of triclosan and 100ng of LPS for 24hrs after which supernatants were used to quantify IL8, IL1α, and TNFα. Data are presented as stimulated concentrations minus un-stimulated concentrations. (D) Cell viability of THP1, HPLF, and HOK was evaluated 0, 6 and 24hrs following treatment with 0.75ug/ml of triclosan. 1.0% Triton-X-100 was used to induce lysis in all cell types as a positive control. All assays were performed five times.
Figure 2
Figure 2. Pre-exposure of HOK to triclosan perturbs LPS-induced inflammation while augmenting LPS-induced anti-microbial responses
HOK were pretreated with 0.75ug/ml of triclosan for 24hrs after which they were left un-stimulated or were stimulated with 100ng of LPS for an additional 24hrs. Supernatants were used to quantify (A) IL8, IL1α, and TNFα, along with (B) βD2 and βD3 *p value <0.05. ANOVA with Bonferroni’s Multiple Comparisons. All assays were performed five times.
Figure 3
Figure 3. Triclosan regulates TLR signaling by down regulation of TRAF6 and IRAK1 expression and de novo synthesis of regulatory miRNA 146a [mir146a]
HOK were pretreated with 0.75ug/ml of triclosan for 24hrs after which they were stimulated with 100ng of LPS for an additional 0, 6 or 24hrs. (A) mRNA was used to quantify tlr4 copy number (B–C) cellular protein was used to determine IRAK1 and TRAF6 expression and (D) total RNA was probed for miR146a expression. (E) Kinteics of TRAF6 and IRAK1 expression were determined by one-phase decay and kinetics of mir146a accumulation was determined by one-phase association. circle = 0.00ug/ml triclosan; square = 0.75ug/ml triclosan *p value <0.05. ANOVA with Bonferroni’s Multiple Comparisons. All assays were performed 3–4 times.
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