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Journal of Dental Research
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Biological

TGF-β1 Inhibits TLR-mediated Odontoblast Responses to Oral Bacteria

O.V. Horst1,2,3, K.A. Tompkins4, S.R. Coats4, P.H. Braham4, R.P. Darveau1,4 and B.A. Dale1,5,6,*

1 Departments of Oral Biology, Box 357132,
2 Endodontics,
3 Dental Public Health Sciences,
4 Periodontics,
5 Biochemistry, and
6 Medicine/Dermatology, University of Washington, Seattle, WA 98195-7132

Correspondence: bdale{at}u.washington.edu

TGF-β1 exerts diverse functions in tooth development and tissue repair, but its role in microbial defenses of the tooth is not well-understood. Odontoblasts extending their cellular processes into the dentin are the first cells to recognize signals from TGF-β1 and bacteria in carious dentin. This study aimed to determine the role of TGF-β1 in modulating odontoblast responses to oral bacteria. We show that these responses depend upon the expression levels of microbial recognition receptors TLR2 and TLR4 on the cell surface. Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum activated both TLRs, but TLR4 played a greater role. Lack of cell-surface TLR2 was associated with poor response to Streptococcus mutans, Enterococcus faecalis, and Lactobacillus casei. TGF-β1 inhibited TLR2 and TLR4 expression and attenuated odontoblast responses. Our findings suggest that the balance between TLR-mediated inflammation and TGF-β1 anti-inflammatory activity plays an important role in pulpal inflammation.

Key Words: Toll-like receptors • transforming growth factor beta 1 • odontoblasts • chemokines • pro-inflammatory cytokines

Journal of Dental Research, Vol. 88, No. 4, 333-338 (2009)
DOI: 10.1177/0022034509334846
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