Premium
Locally administered interferon‐γ accelerates lipopolysaccharide‐induced osteoclastogenesis independent of immunohistological RANKL upregulation
Author(s) -
Ayon Haro E. R.,
Ukai T.,
Yokoyama M.,
Kishimoto T.,
Yoshinaga Y.,
Hara Y.
Publication year - 2011
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2011.01352.x
Subject(s) - rankl , osteoclast , lipopolysaccharide , bone resorption , downregulation and upregulation , in vivo , in vitro , chemistry , endocrinology , medicine , interferon , macrophage , cytokine , macrophage colony stimulating factor , resorption , immunology , biology , receptor , biochemistry , activator (genetics) , microbiology and biotechnology , gene
Ayon Haro ER, Ukai T, Yokoyama M, Kishimoto T, Yoshinaga Y, Hara Y. Locally administered interferon‐γ accelerates lipopolysaccharide‐induced osteoclastogenesis independent of immunohistological RANKL upregulation. J Periodont Res 2011; 46: 361–373. © 2011 John Wiley & Sons A/SBackground and Objective: Interferon‐γ (IFN‐γ) potently inhibits RANKL‐induced osteoclastogenesis in vitro . In contrast, previous studies have shown that an increase in IFN‐γ expression is correlated with an increase in lipopolysaccharide (LPS)‐induced bone loss in vivo . However, it is not clear whether local IFN‐γ accelerates osteoclastogenesis or not in vivo . Therefore, the aim of this study was to clarify the role of local IFN‐γ in LPS‐induced osteoclastogenesis. Material and Methods: We induced bone loss in calvaria by injecting LPS. One group of mice received an IFN‐γ injection together with LPS injection, while another group received IFN‐γ 2 d after LPS injection. Bone resorption was observed histologically. Next, we stimulated murine bone marrow macrophages with macrophage‐colony stimulating factor and RANKL in vitro . We added different doses of IFN‐γ and/or LPS at 0 or 48 h time points. Cells were stained with tartrate‐resistant acid phosphatase at 72 h. Results: Local administration of IFN‐γ together with LPS injection did not affect osteoclast formation. However, IFN‐γ injected after LPS injection accelerated osteoclast formation. Also, we confirmed that IFN‐γ added at 0 h inhibited RANKL‐induced osteoclastogenesis in vitro . However, inhibition by IFN‐γ added at 48 h was reduced compared with that by IFN‐γ added at 0 h. Interestingly, IFN‐γ together with a low concentration of LPS accelerated osteoclast formation when both were added at 48 h compared with no addition of IFN‐γ. Conclusion: The results suggest that local IFN‐γ accelerates osteoclastogenesis in certain conditions of LPS‐induced inflammatory bone loss.