Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts.
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 (OSMR beta), 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 OSMR beta expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease.
Hosokawa
Yoshitaka
Y
Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan. hosokawa@dent.tokushima-u.ac.jp
Hosokawa
Ikuko
I
Ozaki
Kazumi
K
Nakanishi
Tadashi
T
Nakae
Hideaki
H
Matsuo
Takashi
T
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives / Q000494:pharmacology*; D002478:Cells, Cultured; D054357:Chemokine CXCL10 / Q000378:metabolism*; D050822:Cytokine Receptor gp130 / Q000235:genetics / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D005881:Gingiva / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D053683:Oncostatin M / Q000494:pharmacology*; D053681:Oncostatin M Receptor beta Subunit / Q000235:genetics / Q000378:metabolism; D009994:Osmolar Concentration; D010510:Periodontal Diseases / Q000517:prevention & control; D010766:Phosphorylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D004791:Enzyme Inhibitors; C494199:IL6ST protein, human; C508348:OSMR protein, human; D053681:Oncostatin M Receptor beta Subunit; D053683:Oncostatin M; D050822:Cytokine Receptor gp130; D002392:Catechin; C062669:epicatechin gallate; C045651:epigallocatechin gallate