IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice

Abstract EN

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.