Hosokawa Yoshitaka, Hosokawa Ikuko, Ozaki Kazumi, Nakanishi Tadashi, Nakae Hideaki, Matsuo Takashi
Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Japan.
Cell Physiol Biochem. 2009;24(5-6):391-6. doi: 10.1159/000257431. Epub 2009 Nov 4.
CC chemokine ligand 20 (CCL20) plays a pivotal role in the recruitment of Th17 cells and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, have multiple beneficial effects, but the effects of catechins on CCL20 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit interleukin (IL)-17A-induced CCL20 production in human gingival fibroblasts. IL-17A increased CCL20 production in HGFs in a concentration-dependent manner. EGCG and ECG prevented IL-17A-mediated CCL20 production in HGFs. Inhibitors of p38 mitogen-activated protein kinase (MAPK) or extracellular signal-regulated kinase (ERK) decreased IL-17A-induced CCL20 production. EGCG and ECG prevented IL-17A-induced phosphorylation of p38 MAPK and ERK in HGFs. In addition, EGCG and ECG attenuated IL-17 receptor expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids catechins could be used to provide direct benefits in periodontal disease.
CC趋化因子配体20(CCL20)在Th17细胞的募集以及牙周疾病的发展过程中起着关键作用。表没食子儿茶素没食子酸酯(EGCG)和表儿茶素没食子酸酯(ECG)是绿茶中的主要儿茶素,具有多种有益作用,但儿茶素对人牙龈成纤维细胞(HGFs)中CCL20产生的影响尚不清楚。在本研究中,我们探究了EGCG和ECG抑制白细胞介素(IL)-17A诱导的人牙龈成纤维细胞中CCL20产生的机制。IL-17A以浓度依赖性方式增加HGFs中CCL20的产生。EGCG和ECG可阻止IL-17A介导的HGFs中CCL20的产生。p38丝裂原活化蛋白激酶(MAPK)或细胞外信号调节激酶(ERK)的抑制剂可降低IL-17A诱导的CCL20产生。EGCG和ECG可阻止IL-17A诱导的HGFs中p38 MAPK和ERK的磷酸化。此外,EGCG和ECG可减弱HGFs上IL-17受体的表达。这些数据提供了一种新机制,通过该机制绿茶类黄酮儿茶素可用于在牙周疾病中带来直接益处。