Oncostatin M synergistically induces CXCL10 and ICAM-1 expression in IL-1β-stimulated-human gingival fibroblasts

✍ Scribed by Yoshitaka Hosokawa; Ikuko Hosokawa; Kazumi Ozaki; Hideaki Nakae; Takashi Matsuo

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 349 KB
• Volume: 111
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.22648

✦ Synopsis

Abstract

Periodontitis is a chronic bacterial infection of tooth‐supporting structures. T‐helper type 1 (Th1) cells are related to the exacerbation of periodontal disease. Human gingival fibroblasts (HGFs), the major cell type in periodontal connective tissues, are involved in immunological response in periodontal tissues. However, it is uncertain whether HGFs are related to Th1 response. Chemokine (C‐X‐C motif) ligand 10 (CXCL10) is a cytokine, that is related to Th1 cells migration. Intercellular adhesion molecule (ICAM)‐1 is involved in Th1 cells retention and activation in inflamed tissue. The aim of this study is to examine the effect of oncostatin M (OSM) on CXCL10 and ICAM‐1 expression in HGFs. OSM stimulation induced CXCL10 and ICAM‐1 expression in HGFs. Moreover, the synergistic effects of CXCL10 release and ICAM‐1 expression in HGFs were observed with combined stimulation of interleukin (IL)‐1β and OSM. OSM increased type 1 IL‐1 receptor (IL‐1R1) expression, and IL‐1β enhanced OSMRβ expression on HGFs. IL‐1β + OSM stimulation enhanced the phosphorylation of inhibitor of nuclear factor κB (IκB)‐α, signal transducer and activator of transcription (STAT)3, c‐Jun N terminal kinase (JNK), and protein kinase B (Akt) compared to OSM or IL‐1β stimulation. CXCL10 production from OSM + IL‐1β stimulated HGFs was suppressed by nuclear factor (NF)‐κB, STAT3, JNK, and phosphoinositide‐3‐kinase (PI3K) inhibitors. On the other hand, only NF‐κB and STAT3 inhibitors suppressed ICAM‐1 expression enhanced by OSM + IL‐1β treatment. These effects of OSM and IL‐1β may promote Th1 cells infiltration and retention in periodontally diseased tissues and be related to exacerbation of periodontal disease. J. Cell. Biochem. 111: 40–48, 2010. © 2010 Wiley‐Liss, Inc.