Effect of globular adiponectin on interleukin-6 and interleukin-8 expression in periodontal ligament and gingival fibroblasts.
10.5051/jpis.2011.41.3.149
- Author:
Hong Gyu PARK
1
;
Eun Jung BAK
;
Ji Hye KIM
;
Yang Sin LEE
;
Seong Ho CHOI
;
Jeong Heon CHA
;
Yun Jung YOO
Author Information
1. Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry, Seoul, Korea. yu618@yuhs.ac
- Publication Type:Original Article
- Keywords:
Adiponectin;
Periodontal ligament;
Fibroblasts;
Receptors;
Cytokines
- MeSH:
Adiponectin;
Adipose Tissue;
Blotting, Western;
Cytokines;
Escherichia coli;
Fibroblasts;
Humans;
Interleukin-6;
Interleukin-8;
Interleukins;
Periodontal Ligament;
Polymyxin B;
Receptors, Adiponectin;
RNA, Messenger
- From:Journal of Periodontal & Implant Science
2011;41(3):149-156
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Globular adiponectin (gAd) is a type of adipocytokine, which is mainly produced by adipose tissue. It has been reported that gAd acts as a pro- as well as an anti-inflammatory factor. Interleukin (IL)-6 and IL-8 are pro-inflammatory cytokines. To investigate the role of gAd on periodontal tissues, the expression of adiponectin receptor 1 (AdipoR1) and the effect of gAd on the expression of IL-6 and IL-8 were investigated in periodontal ligament (PDL) and gingival fibroblasts. METHODS: PDL and gingival fibroblasts were cultured from human periodontal tissues. gAd derived from Escherichia coli and murine myeloma cells were used. The expression of AdipoR1 was estimated by reverse transcription-polymerase chain reaction and western blot. The expression of cytokines was measured by enzyme-linked immunosorbent assay. RESULTS: PDL and gingival fibroblasts expressed both mRNA and protein of AdipoR1. gAd derived from E. coli increased the production of IL-6 and IL-8, but polymyxin B, an inhibitor of lipopolysaccharide (LPS), inhibited IL-6 and IL-8 production induced by gAd in both types of cells. gAd derived from murine myeloma cells did not induce IL-6 and IL-8 production in those cells. gAd derived from E. coli contained higher levels of LPS than gAd derived from murine myeloma cells. LPS increased production of IL-6 and IL-8 in PDL and gingival fibroblasts, but pretreatment of cells with gAd derived from murine myeloma cells did not inhibit LPS-induced IL-6 and IL-8 expression. CONCLUSIONS: Our results suggest that PDL and gingival fibroblasts express AdipoR1 and that gAd does not act as a modulator of IL-6 and IL-8 expression in PDL and gingival fibroblasts.
