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10.1155/2015/214878

http://scihub22266oqcxt.onion/10.1155/2015/214878
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C4433692!4433692!26064997
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suck abstract from ncbi


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pmid26064997      J+Immunol+Res 2015 ; 2015 (ä): ä
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  • IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice #MMPMID26064997
  • Yoshimatsu M; Kitaura H; Fujimura Y; Kohara H; Morita Y; Yoshida N
  • J Immunol Res 2015[]; 2015 (ä): ä PMID26064997show ga
  • Lipopolysaccharide (LPS) is related to osteoclastogenesis in osteolytic diseases. Interleukin- (IL-) 12 is an inflammatory cytokine that plays a critical role in host defense. In this study, we investigated the effects of IL-12 on LPS-induced osteoclastogenesis. LPS was administered with or without IL-12 into the supracalvariae of mice, and alterations in the calvarial suture were evaluated histochemically. The number of osteoclasts in the calvarial suture and the mRNA level of tartrate-resistant acid phosphatase (TRAP), an osteoclast marker, were lower in mice administered LPS with IL-12 than in mice administered LPS alone. The serum level of tartrate-resistant acid phosphatase 5b (TRACP 5b), a bone resorption marker, was also lower in mice administered LPS with IL-12 than in mice administered LPS alone. These results revealed that IL-12 might inhibit LPS-induced osteoclastogenesis and bone resorption. In TdT-mediated dUTP-biotin nick end-labeling (TUNEL) assays, apoptotic changes in cells were recognized in the calvarial suture in mice administered LPS with IL-12. Furthermore, the mRNA levels of both Fas and FasL were increased in mice administered LPS with IL-12. Taken together, the findings demonstrate that LPS-induced osteoclastogenesis is inhibited by IL-12 and that this might arise through apoptotic changes in osteoclastogenesis-related cells induced by Fas/FasL interactions.
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