模式识别受体和病原体相关分子模式及其在牙周病防御中的作用
Effects of pattern recognition receptors and pathogen associated molecular patterns in defense of periodontal disease

摘要： 模式识别受体（PRR）是宿主抵抗病原微生物的感应器，可识别一种或多种病原体相关分子模式（PAMP），可及时向下游通路转导信号，引发先天性免疫反应。PAMP包括脂多糖（LPS）、脂磷壁酸、肽聚糖和甘露糖等。不同的PAMP可被不同的Toll样受体（TLR）识别或组合识别，然后通过一系列蛋白质级联反应激活细胞因子，从而有效地活化天然免疫系统。PAMP作用于TLR后，可促进炎性细胞因子的合成与释放；诱导一氧化氮依赖性杀菌活性和呼吸爆发；介导由细菌脂蛋白引起的人单核细胞系和表达TLR2的上皮细胞系程序性细胞死 亡；LPS通过作用于TLR4促进树突细胞成熟，诱导TLR2的合成与表达，进而分泌白细胞介素-6等细胞因子。对TLR的研究将有助于认识慢性牙周病并为其治疗提供新的方法，故本文就牙龈上皮表面的PRR和牙周致病菌表面的PAMP及其在牙周病中的防御作用等研究进展作一综述。
Abstract: Pattern recognition receptors(PRR) can sense the presence of microorganisms by recognizing pathogenassociated molecular patterns(PAMP), and timely transduce signals to downstream pathways and lead to inflammasome generation. PAMP include lipopolysaccharide (LPS), lipoteichoicacid, peptidoglycan, and teichoic acid mannose. Different PAMP can be recognized by different PRR, and trigger cytokines through serious of protein cascade reaction so as to effectively revitalizing natural immune response. After recognized by Toil-like receptor(TLR), PAMP can contribute to the synthesis and release of proinflammatory cytokines, induce nitric oxide dependency bactericidal activity and breath, and mediate human monocyte cell and epithelium cell expressing TLR2 apoptosis. After effected by TLR4, LPS can promote dendritic cells mature, induce the synthesis and release of TLR2, and secrete cytokines such as interleukin-6. Studying TLR will contribute to the understanding of chronic periodontal disease and provide new methods of the treatment. Therefore, research progress of the gingival epithelial PRR and PAMP on the surface of periodontal pathogens, as well as their function in periodontal disease, is reviewed in this paper.
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