Cutting edge:: TLR2 is required for the innate response to Porphyromonas gingivalis:: activation leads to bacterial persistence and TLR2 deficiency attenuates induced alveolar bone resorption
Cutting edge:: TLR2 is required for the innate response to Porphyromonas gingivalis:: activation leads to bacterial persistence and TLR2 deficiency attenuates induced alveolar bone resorption
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DOI：
10.4049/jimmunol.177.12.8296
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发表时间：
2006-12-15
影响因子：
4.4
通讯作者：
Nussbaum, Gabriel
中科院分区：
文献类型：
--
作者：
Burns, Elia;Bachrach, Gilad;Nussbaum, Gabriel
牙周炎是一种慢性炎症性疾病，导致牙齿附着装置的破坏。特定口腔细菌的存在和宿主炎症反应有助于疾病进展。牙龈卟啉单胞菌是一种革兰氏阴性厌氧菌，被认为是一种主要的牙周病原体。从牙龈卟啉单胞菌分离的Ag通过TLR2或TLR4激活先天免疫细胞。我们用活的牙龈卟啉单胞菌攻击TLR2和TLR4缺陷小鼠，并研究炎症反应和细菌存活。野生型和TLR4缺陷小鼠响应牙龈卟啉单胞菌攻击产生高水平的细胞因子，而细胞因子水平在TLR2缺陷小鼠中几乎不存在或延迟。令人惊讶的是，牙龈卟啉单胞菌在TLR2缺陷小鼠中被清除得更快。此外，TLR2缺陷小鼠抵抗口腔感染牙龈卟啉单胞菌后的骨丢失。
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, Wildtype 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.