Locally administered T cells from mice immunized with lipopolysaccharide (LPS) accelerate LPS-induced bone resorption
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- 作者：Yukio Ozaki ; Takashi Ukai ; Masayuki Yamaguchi ; Miho Yokoyama ; Esperanza R. Ayó ; n Haro ; Mayumi Yoshimoto ; Takashi Kaneko ; Miho Yoshinaga ; Hirotaka Nakamura ; Chiaki Shiraishi ; Yoshitaka Hara
- 关键词：T cell ; Bone resorption ; Osteoclast ; Lipopolysaccharide ; Tumor necrosis factor-α
- 刊名：Bone
- 出版年：2009
- 出版时间：June 2009
- 年：2009
- 卷：44
- 期：6
- 页码：1169-1176
- 全文大小：1794 K
文摘
T cells play important roles in bone destruction and osteoclastogenesis and are found in chronic destructive bone lesions. Lipopolysaccharide (LPS) is one of several pathological factors involved in inflammatory bone destruction. We previously described the importance of T cells in the inflammatory bone resorption that occurs after repeated LPS administration. However, whether local or systemic T cells are important for inflammatory bone resorption and whether immunization of host animals influences bone resorption remain unclear. The present study examines the effects of local extant T cells from LPS-immunized mice on LPS-induced bone resorption. T cells from LPS-immunized or non-immunized mice were injected together with LPS into the gingival tissues of mice with severe combined immunodeficiency disease that lack both T and B cells. We histomorphometrically evaluated bone resorption at sites of T cell injections and examined the influence of T cells from LPS-immunized mice on osteoclastogenesis in vitro. We found that locally administered T cells from LPS-immunized but not non-immunized mice accelerated LPS-induced bone resorption in vivo. Moreover, T cells from LPS-immunized mice increased osteoclastogenesis in vitro induced by receptor activator of NF-κ B ligand and LPS and anti-tumor necrosis factor (TNF)-α antibody inhibited this increase. These results demonstrated that local extant T cells accelerate inflammatory bone resorption. Furthermore, T cells from LPS-immunized mice appear to elevate LPS-induced bone resorption using TNF-α.