IL-12 inhibits lipopolysaccharide stimulated osteoclastogenesis in mice

Masako Yoshimatsu, Hideki Kitaura, Yuji Fujimura, Haruka Kohara, Yukiko Morita, Noriaki Yoshida

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number214878
JournalJournal of immunology research
Volume2015
DOIs
Publication statusPublished - 2015

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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