NDLI: Interleukin-1 receptor-associated kinase-4 (IRAK4) promotes inflammatory osteolysis by activating osteoclasts and inhibiting formation of foreign body giant cells.

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Interleukin-1 receptor-associated kinase-4 (IRAK4) promotes inflammatory osteolysis by activating osteoclasts and inhibiting formation of foreign body giant cells.

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Interleukin-1 receptor-associated kinase-4 (IRAK4) promotes inflammatory osteolysis by activating osteoclasts and inhibiting formation of foreign body giant cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fujie, Atsuhiro Miyamoto, Kana Tando, Toshimi Matsumoto, Morio Morioka, Hideo Katsuyama, Eri Watanabe, Ryuichi Morita, Mayu Miyamoto, Hiroya Miyamoto, Takeshi Toyama, Yoshiaki Kobayashi, Tami Sato, Yuiko Niki, Yasuo Kanagawa, Hiroya Hao, Wu
Description	Author Affiliation: Katsuyama E ( From the Departments of Orthopedic Surgery.); Miyamoto H ( From the Departments of Orthopedic Surgery.); Kobayashi T ( From the Departments of Orthopedic Surgery, Integrated Bone Metabolism and Immunology.); Sato Y ( From the Departments of Orthopedic Surgery, Musculoskeletal Reconstruction and Regeneration Surgery, and.); Hao W ( From the Departments of Orthopedic Surgery.); Kanagawa H ( From the Departments of Orthopedic Surgery.); Fujie A ( From the Departments of Orthopedic Surgery.); Tando T ( From the Departments of Orthopedic Surgery.); Watanabe R ( From the Departments of Orthopedic Surgery.); Morita M ( Dentistry and Oral Surgery, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan.); Miyamoto K ( From the Departments of Orthopedic Surgery.); Niki Y ( From the Departments of Orthopedic Surgery.); Morioka H ( From the Departments of Orthopedic Surgery.); Matsumoto M ( From the Departments of Orthopedic Surgery.); Toyama Y ( From the Departments of Orthopedic Surgery.); Miyamoto T ( From the Departments of Orthopedic Surgery, Integrated Bone Metabolism and Immunology, miyamoto@z5.keio.jp.)
Abstract	Formation of foreign body giant cells (FBGCs) occurs following implantation of medical devices such as artificial joints and is implicated in implant failure associated with inflammation or microbial infection. Two major macrophage subpopulations, M1 and M2, play different roles in inflammation and wound healing, respectively. Therefore, M1/M2 polarization is crucial for the development of various inflammation-related diseases. Here, we show that FBGCs do not resorb bone but rather express M2 macrophage-like wound healing and inflammation-terminating molecules in vitro. We also found that FBGC formation was significantly inhibited by inflammatory cytokines or infection mimetics in vitro. Interleukin-1 receptor-associated kinase-4 (IRAK4) deficiency did not alter osteoclast formation in vitro, and IRAK4-deficient mice showed normal bone mineral density in vivo. However, IRAK4-deficient mice were protected from excessive osteoclastogenesis induced by IL-1ß in vitro or by LPS, an infection mimetic of Gram-negative bacteria, in vivo. Furthermore, IRAK4 deficiency restored FBGC formation and expression of M2 macrophage markers inhibited by inflammatory cytokines in vitro or by LPS in vivo. Our results demonstrate that osteoclasts and FBGCs are reciprocally regulated and identify IRAK4 as a potential therapeutic target to inhibit stimulated osteoclastogenesis and rescue inhibited FBGC formation under inflammatory and infectious conditions without altering physiological bone resorption.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	2
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-01-09
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Genetics Giant Cells, Foreign-Body Metabolism Inflammation Interleukin-1 Receptor-Associated Kinases Animals Bone Resorption Gene Expression Regulation, Developmental Pathology Macrophages Mice Osteoclasts Osteolysis Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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