Type 1 Diabetes–associated TLR Responsiveness of Oral Epithelial Cells

In type 1 diabetes (T1D), a Toll-like receptor (TLR)-hyper-inflammatory monocytic phenotype has been implicated as a mechanism of exacerbated tissue destruction. Other cells of the periodontium, including oral epithelial cells (OECs), express innate immune receptors, including TLRs. To delineate the...

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Bibliographic Details
Published in:Journal of dental research 2014-02, Vol.93 (2), p.169-174
Main Authors: Neiva, K.G., Calderon, N.L., Alonso, T.R., Panagakos, F., Wallet, S.M.
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Anti-Inflammatory Agents - pharmacology
Cell Culture Techniques
Cells, Cultured
Dentistry
Diabetes Mellitus, Type 1 - immunology
Epithelial Cells - immunology
Humans
Immunity, Innate - immunology
Inflammation Mediators - analysis
Interleukin-8 - analysis
Ligands
Lipopolysaccharides - immunology
Macrophages - immunology
MicroRNAs - analysis
Middle Aged
Mouth Mucosa - cytology
Mouth Mucosa - immunology
Phenotype
Porphyromonas gingivalis - immunology
Research Reports
Toll-Like Receptor 1 - analysis
Toll-Like Receptor 2 - analysis
Toll-Like Receptor 4 - analysis
Toll-Like Receptor 6 - analysis
Toll-Like Receptors - immunology
Transforming Growth Factor beta1 - analysis
Triclosan - pharmacology
Young Adult
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Summary:In type 1 diabetes (T1D), a Toll-like receptor (TLR)-hyper-inflammatory monocytic phenotype has been implicated as a mechanism of exacerbated tissue destruction. Other cells of the periodontium, including oral epithelial cells (OECs), express innate immune receptors, including TLRs. To delineate the TLR responses of OECs derived from T1D participants and to determine effects of the anti-inflammatory agent triclosan on the TLR-hyper-inflammatory phenotype, primary human OECs from individuals with T1D and diabetes-free individuals were stimulated with TLR ligands in the presence and/or absence of triclosan. The expression of pro-inflammatory cytokines and micro-RNAs (miRNAs) was evaluated. While the repertoire of TLRs expressed by OECs is similar to that expressed by macrophages (Mϕ), the relative amounts and ratios are significantly different. OECs demonstrate a TLR-response profile similar to that of Mϕ, yet attenuated. OECs have a unique response to P. gingivalis LPS, where miR146a and miR155 play a regulatory role in responsiveness. OECs from T1D participants are TLR-hyper-responsive, due to dysregulated induction of miR146a and miR155, which is abrogated by pre-treatment with triclosan. The aberrant TLR-activation of OECs in T1D has the potential to contribute to excessive soft- and hard-tissue destruction. Importantly, triclosan’s anti-inflammatory property is effective in abrogating TLR-induced OEC hyperactivity.
ISSN:0022-0345
1544-0591
DOI:10.1177/0022034513516345