The bacterium Porphyromonas gingivalis gets most of the blame for periodontal disease, which erodes bone that supports teeth and is the leading cause of tooth loss. P gingivalis adheres to oral surfaces using molecules such as lipopolysaccharides (LPS) and lipoproteins. These molecules are recognized by Toll-like receptors (TLRs) that are expressed on cells of the immune system: TLR2 binds bacterial lipopeptides and TLR4 binds LPS. Burns and colleagues tested how these TLRs are involved in the host mouse response against P gingivalis. They implanted metal coils subcutaneously and injected bacteria into the lumen, and then sampled the space at later times to monitor the immune response in wild-type (WT), TLR2, and -4 knockout (-/-) mice. They observed differences in the induction of cytokines, most dramatically a reduced accumulation of TNF, interferon-gamma, and interleukin-10 in TLR2-/- mice. Surprisingly, TLR2-/- mice cleared the bacteria from the injection site and blood within a day. In contrast, bacteria remained in the blood of WT and TLR4-/- mice for at least 4 days. Moreover, when mice were orally challenged with P. gingivalis, significant bone loss resulted within 6 weeks in WT but not TLR2-/- mice (Figure). Would blocking TLR2 with lipopeptides in a mouthwash or chewing gum help protect teeth?
J Immunol. 2006 Dec 15;177(12):8296-300. "TLR2 is required for the innate response to Porphyromonas gingivalis: activation leads to bacterial persistence and TLR2 deficiency attenuates induced alveolar bone resorption." Burns E, Bachrach G, Shapira L, Nussbaum G.
Wednesday, February 28, 2007
TLR2 Helps Bacteria Weaken Gums
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TLR2 was implicated also in the erosion of bone observed in rheumatoid arthritis (RA). De Rycke and colleagues showed that RA therapy with TNF blocker also downregulates TLR2 and TLR4 expression locally in the joint and systemically. Sacre and colleagues showed that TLR signaling adapter proteins MyD88 and Mal/TIRAP contribute to the joint inflammation and destruction in RA.
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