Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts

Hosokawa, Yoshitaka; Hosokawa, Ikuko; Ozaki, Kazumi; Nakanishi, Tadashi; Nakae, Hideaki; Matsuo, Takashi

doi:10.1016/j.jnutbio.2009.04.005

« PreviousThe Journal of Nutritional Biochemistry
Volume 21, Issue 7 , Pages 659-664, July 2010

Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts

Yoshitaka Hosokawa
- Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan
- Corresponding author. Tel.: +81 886 33 7340; fax: +81 886 33 7340.
Ikuko Hosokawa
- Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan
Kazumi Ozaki
- Department of Oral Health Care Promotion, School of Oral Health and Welfare, Faculty of Dentistry, The University of Tokushima, Tokushima 770-8504, Japan
Tadashi Nakanishi
- Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan
Hideaki Nakae
- Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan
Takashi Matsuo
- Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan

Received 21 November 2008; received in revised form 6 April 2009; accepted 13 April 2009. published online 21 July 2009.

Abstract

CXC chemokine ligand 10 (CXCL10) plays a pivotal role in the recruitment of Th1 cells and, thus, in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins derived from green tea, have multiple beneficial effects, but the effects of catechins on CXCL10 production from human gingival fibroblasts (HGFs) is not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit oncostatin M (OSM)-induced CXCL10 production in HGFs. HGFs constitutively expressed glycoprotein 130 and OSM receptor beta (OSMRβ), which are OSM receptors. OSM increased CXCL10 production in a concentration-dependent manner. EGCG and ECG prevented OSM-mediated CXCL10 production by HGFs. Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription (STAT)3 decreased OSM-induced CXCL10 production. EGCG significantly prevented OSM-induced phosphorylation of JNK, Akt (Ser473) and STAT3 (Tyr705 and Ser727). ECG prevented phosphorylation of JNK and Akt (Ser473). In addition, EGCG and ECG attenuated OSMRβ expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease.

Keywords: Catechins, Oncostatin M, CXCL10, Human gingival fibroblasts