School of Dentistry, Center for Oral and Systemic Diseases, North Carolina Oral Health Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27709, USA.
J Clin Periodontol. 2010 May;37(5):412-8. doi: 10.1111/j.1600-051X.2010.01548.x.
We sought to determine whether triclosan (2,4,4'-trichloro-2'-hydroxydiphenylether), an extensively used anti-plaque agent with broad-spectrum anti-microbial activity, with reported anti-inflammatory effects via inhibition of prostaglandin E2 and interleukin 1 (IL-1)beta, could also more broadly suppress multiple inflammatory gene pathways responsible for the pathogenesis of gingivitis and periodontitis.
As an exploratory study, the effects of triclosan on the inflammatory gene expression profile were assessed ex vivo using peripheral whole blood samples from eight periodontally healthy donors. Ten-millilitres whole blood aliquots were incubated 2 h with 0.3 microg/ml Escherichia coli lipopolysaccharide (LPS) with or without 0.5 microg/ml triclosan. Affymetrix microarray gene expression profiles from isolated leucocytes and pathway-specific quantitative polymerase chain reaction arrays were used to investigate changes in expression of target cytokines and cell signalling molecules.
Ex vivo human whole blood assays indicated that triclosan significantly down-regulated the LPS-stimulated expression of Toll-like receptor signalling molecules and other multiple inflammatory molecules including IL-1 and IL-6 and the dampening of signals that activate the T-helper type 1 acquired immune response via suppression of CD70 with concomitant up-regulation of growth factors related to bone morphogenetic protein (BMP)2 and BMP6 synthesis.
Anti-inflammatory effects were found in this exploratory survey, including suppression of microbial-pathogen recognition pathway molecules and the suppression of acute and chronic mediators of inflammation.
我们旨在确定三氯生（2,4,4'-三氯-2'-羟基二苯醚）是否具有广谱抗菌活性，是否可以通过抑制前列腺素 E2 和白细胞介素 1（IL-1）β来发挥抗炎作用，是否也可以更广泛地抑制导致牙龈炎和牙周炎发病机制的多个炎症基因途径。
作为一项探索性研究，使用来自 8 名牙周健康供体的外周全血样本，在体外评估三氯生对炎症基因表达谱的影响。用 10 毫升全血等分试样与 0.3 微克/毫升大肠杆菌脂多糖（LPS）孵育 2 小时，并用 0.5 微克/毫升三氯生处理。使用分离的白细胞的 Affymetrix 微阵列基因表达谱和途径特异性定量聚合酶链反应阵列来研究靶细胞因子和细胞信号分子表达的变化。
体外人全血测定表明，三氯生可显著下调 LPS 刺激的 Toll 样受体信号分子和其他多种炎症分子的表达，包括 IL-1 和 IL-6，并通过抑制 CD70 抑制 T 辅助 1 获得性免疫反应的信号，同时上调与骨形态发生蛋白（BMP）2 和 BMP6 合成相关的生长因子。
在这项探索性调查中发现了抗炎作用，包括抑制微生物病原体识别途径分子和抑制急性和慢性炎症介质。
