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代谢组学揭示牙周病中大分子降解的升高。

Metabolomics reveals elevated macromolecular degradation in periodontal disease.

机构信息

Colgate-Palmolive Technology Center, 909 River Road, Piscataway, NJ 08855, USA.

出版信息

J Dent Res. 2011 Nov;90(11):1293-7. doi: 10.1177/0022034511416240. Epub 2011 Aug 19.

Abstract

Periodontitis is a chronic inflammatory disease characterized by tissue destruction. In the diseased oral environment, saliva has primarily been considered to act as a protectant by lubricating the tissue, mineralizing the bones, neutralizing the pH, and combating microbes. To understand the metabolic role that saliva plays in the diseased state, we performed untargeted metabolomic profiling of saliva from healthy and periodontitic individuals. Several classes of biochemicals, including dipeptide, amino acid, carbohydrate, lipids, and nucleotide metabolites, were altered, consistent with increased macromolecular degradation of proteins, triacylglycerol, glycerolphospholipids, polysaccharides, and polynucleotides in the individuals with periodontal disease. These changes partially reflected the enhanced host-bacterial interactions in the diseased state as supported by increased levels of bacterially modified amino acids and creatine metabolite. More importantly, the increased lipase, protease, and glycosidase activities associated with periodontitis generated a more favorable energy environment for oral bacteria, potentially exacerbating the disease state.

摘要

牙周炎是一种以组织破坏为特征的慢性炎症性疾病。在患病的口腔环境中,唾液主要被认为是通过润滑组织、矿化骨骼、中和 pH 值以及抵御微生物来发挥保护作用。为了了解唾液在患病状态下的代谢作用,我们对健康和牙周炎个体的唾液进行了非靶向代谢组学分析。包括二肽、氨基酸、碳水化合物、脂质和核苷酸代谢物在内的几类生化物质发生了改变,这与牙周病个体中蛋白质、甘油三酯、甘油磷脂、多糖和多核苷酸的大分子降解增加一致。这些变化部分反映了患病状态下宿主-细菌相互作用的增强,这得到了细菌修饰氨基酸和肌酸代谢物水平升高的支持。更重要的是,与牙周炎相关的脂肪酶、蛋白酶和糖苷酶活性的增加为口腔细菌创造了更有利的能量环境,可能使疾病恶化。

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