Institute of Dental Sciences, Faculty of Dental Medicine, Hadassah and Hebrew University Medical Center, Jerusalem, Israel.
J Immunol. 2010 Feb 1;184(3):1455-62. doi: 10.4049/jimmunol.0900378. Epub 2009 Dec 30.
Porphyromonas gingivalis is a gram-negative anaerobe considered to be a major periodontal pathogen. TLR2 plays a central role in the response to P. gingivalis infection in vivo. In its absence there is a weak inflammatory response; however, bacteria are cleared rapidly compared with wild-type mice. We examined the role of the TLR adaptor proteins MyD88 and TLR/IL-1R-domain-containing adaptor-inducing IFN-beta in the inflammatory response to P. gingivalis in vivo and in the ability to clear the bacterial infection. Proinflammatory cytokine production in response to P. gingivalis infection depends on TLR2, but it does not require MyD88 or TLR/IL-1R-domain-containing adaptor-inducing IFN-beta. In contrast, the generation of intracellular toxic oxygen species and the ultimate clearance of P. gingivalis infection depend critically on MyD88, independent of TLR2. Thus, robust cytokine production and bacterial clearance are independent events mediated by distinct signaling pathways following infection with P. gingivalis.
牙龈卟啉单胞菌是一种革兰氏阴性厌氧菌，被认为是主要的牙周病原体。TLR2 在体内对牙龈卟啉单胞菌感染的反应中起着核心作用。在缺乏 TLR2 的情况下，炎症反应较弱；然而，与野生型小鼠相比，细菌被迅速清除。我们研究了 TLR 衔接蛋白 MyD88 和 TLR/IL-1R 结构域包含衔接蛋白诱导 IFN-β 在体内对牙龈卟啉单胞菌感染的炎症反应中的作用，以及清除细菌感染的能力。对牙龈卟啉单胞菌感染的反应中促炎细胞因子的产生依赖于 TLR2，但不需要 MyD88 或 TLR/IL-1R 结构域包含衔接蛋白诱导 IFN-β。相比之下，细胞内毒性氧物质的产生和牙龈卟啉单胞菌感染的最终清除严重依赖于 MyD88，与 TLR2 无关。因此，在感染牙龈卟啉单胞菌后，强有力的细胞因子产生和细菌清除是由不同的信号通路介导的独立事件。
