PT  - JOURNAL ARTICLE
AU  - Burns, Elia
AU  - Bachrach, Gilad
AU  - Shapira, Lior
AU  - Nussbaum, Gabriel
TI  - Cutting Edge: TLR2 Is Required for the Innate Response to <em>Porphyromonas gingivalis</em>: Activation Leads to Bacterial Persistence and TLR2 Deficiency Attenuates Induced Alveolar Bone Resorption
AID  - 10.4049/jimmunol.177.12.8296
DP  - 2006 Dec 15
TA  - The Journal of Immunology
PG  - 8296--8300
VI  - 177
IP  - 12
4099  - http://www.jimmunol.org/content/177/12/8296.short
4100  - http://www.jimmunol.org/content/177/12/8296.full
SO  - J. Immunol.2006 Dec 15; 177
AB  - Periodontitis is a chronic inflammatory disease that leads to destruction of the attachment apparatus of the teeth. The presence of particular oral bacteria and the host inflammatory response contribute to disease progression. Porphyromonas gingivalis is a Gram-negative anaerobe considered to be a major periodontal pathogen. Isolated Ags from P. gingivalis activate innate immune cells through TLR2 or TLR4. We challenged TLR2- and TLR4-deficient mice with live P. gingivalis and studied the inflammatory response and bacterial survival. Wild-type and TLR4-deficient mice produced high levels of cytokines in response to P. gingivalis challenge, whereas cytokine levels were nearly absent or delayed in TLR2-deficient mice. Surprisingly, P. gingivalis was cleared far more rapidly in TLR2-deficient mice. In addition, TLR2-deficient mice resisted bone loss following oral infection with P. gingivalis.