Locally administered interferon-γ accelerates lipopolysaccharide-induced osteoclastogenesis independent of immunohistological RANKL upregulation

Abstract

The results suggest that local IFN-γ accelerates osteoclastogenesis in certain conditions of LPS-induced inflammatory bone loss.

The Keap1/Nrf2 Protein Axis Plays a Role in Osteoclast Differentiation by Regulating Intracellular Reactive Oxygen Species Signaling

“…We utilized repeat injections of LPS for our in vivo bone destruction model (32). This bone destruction model induces RANKL-dependent osteoclastogenesis and extensive bone destruction.…”

RANKL induces Bach1 nuclear import and attenuates Nrf2‐mediated antioxidant enzymes, thereby augmenting intracellular reactive oxygen species signaling and osteoclastogenesis in mice

“…Finally, we examined whether Bach1 nuclear export ameliorates RANKL‐dependent bone destruction in vivo . Because repeated LPS injections induce RANKL‐dependent bone destruction in mouse calvaria without any systemic effects (18, 20), the inhibitory effect of Bach1 nuclear export by SFC and ALA on bone destruction was examined. No systemic differences, such as body weight, food intake, and macroscopic observation, were observed between control and LPS injection groups, or between SFC and ALA‐ and vehicle‐injected groups (data not shown).…”

“…Animal experiments were performed in compliance with the Regulations for Animal Experiments and Related Activities at Tsurumi University. We used repeat injections of LPS for our in vivo bone destruction model (18, 20). This bone destruction model induces RANKL‐dependent osteoclastogenesis, and, thus, extensive bone destruction was observed.…”

Reciprocal effects of Interferon‐γ and IL‐4 on differentiation to osteoclast‐like cells by RANKL or LPS

“…Surgical pulp exposure and infection of IFN‐γ‐/‐ mice resulted in no change in bone resorption compared to wild types (Sasaki et al , ). Haro et al showed that local administration of IFN‐γ accelerates LPS‐induced osteoclastogenesis independent of immunohistological RANKL upregulation (Ayon Haro et al , ). Kohara et al , on the other hand, showed that IFN‐γ directly inhibits, by inducing apoptosis, TNF‐α‐induced osteoclastogenesis in vitro and in vivo (Kohara et al , ).…”

“…In comparison with RANKL, the effects of Th1 and Th2 cytokines on LPS‐induced osteoclastogenesis or bone resorption have not been extensively studied. It has been shown that IFN‐γ accelerates osteoclastogenesis in LPS‐induced inflammatory bone loss (Ayon Haro et al , ). Besides blunting osteoclast formation through direct targeting of osteoclast precursors, Gao et al (Gao et al , ) reported that IFN‐γ indirectly stimulates osteoclast formation and bone loss in vivo .…”