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2015 ; 2015
(ä): 214878
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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): 214878
PMID26064997
show 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.