Low Molecular-Weight Curdlan, (1→3)-β-Glucan Suppresses TLR2-Induced RANKL-Dependent Bone Resorption

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  • Aizawa Maki
    Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology
  • Watanabe Kenta
    Institute of Global Innovation Research, Tokyo University of Agriculture and Technology
  • Tominari Tsukasa
    Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology
  • Matsumoto Chiho
    Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology
  • Hirata Michiko
    Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology
  • Grundler Florian M. W.
    Institute of Global Innovation Research, Tokyo University of Agriculture and Technology Institute of Crop Science and Resource Conservation, University of Bonn
  • Inada Masaki
    Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology Institute of Global Innovation Research, Tokyo University of Agriculture and Technology Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology
  • Miyaura Chisato
    Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology Institute of Global Innovation Research, Tokyo University of Agriculture and Technology Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology

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Abstract

<p>Fungal β-glucan is a potent immunological stimulator, and that it activates both the innate immune system and adaptive immunity. Curdlan is (1→3)-β-glucan, a linear form of β-glucan with a high molecular weight; it modulates the immune response. However, its role in bone tissue is controversial, and the effects of curdlan on bone tissues are unknown. Toll-like receptors (TLRs) play critical roles in innate immunity, and various ligands for TLRs are thought to regulate the host defense mechanisms against pathogens. TLR2 is known to form heterodimers with TLR6, and the TLR2-TLR6 heterodimer (TLR2/6) recognizes diacylated lipopeptides from Gram-positive bacteria. In the present study, we prepared low molecular-weight curdlan, (1→3)-β-D-glucan, and examined its effects on bone resorption induced by TLR2/6 signaling. In co-cultures of bone marrow cells and osteoblasts, low molecular-weight curdlan suppressed the osteoclast formation induced by TLR2/6 ligand, and attenuated bone resorption in mouse calvarial organ cultures. Curdlan acted on mouse osteoblasts and suppressed the expression of receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL), a key molecule for osteoclastogenesis. Curdlan also acted on mouse bone marrow macrophages and suppressed RANKL-dependent osteoclast differentiation from osteoclast precursor cells. The present study indicates that low molecular-weight curdlan attenuated TLR2-induced inflammatory bone resorption. Curdlan, (1→3)-β-glucan may be a natural agent with beneficial effects on bone health in humans.</p>

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