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      IL-1 β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes

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          Abstract

          Elevated interleukin (IL)-1 concentrations in synovial fluid have been implicated in joint bone and cartilage destruction. Previously, we showed that IL-1 β stimulated the expression of prostaglandin (PG) receptor EP4 via increased PGE 2 production. However, the effect of IL-1 β on osteoclast formation via chondrocytes is unclear. Therefore, we examined the effect of IL-1 β and/or celecoxib on the expression of macrophage colony-stimulating factor (M-CSF), receptor activator of NF- κB ligand (RANKL), and osteoprotegerin (OPG) in human chondrocytes, and the indirect effect of IL-1 β on osteoclast-like cell formation using RAW264.7 cells. OPG and RANKL expression increased with IL-1 β; whereas M-CSF expression decreased. Celecoxib blocked the stimulatory effect of IL-1 β. Conditioned medium from IL-1 β-treated chondrocytes decreased TRAP staining in RAW264.7 cells. These results suggest that IL-1 β suppresses the formation of osteoclast-like cells via increased OPG production and decreased M-CSF production in chondrocytes, and OPG production may increase through an autocrine mechanism involving celecoxib-related PGs.

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          Osteoblasts and osteoclasts in bone remodeling and inflammation.

          Yosuke Okada, Yoshiya Tanaka, Shingo Nakayamada (2005)
          Bone homeostasis is maintained by a balance between bone resorption by osteoclasts and bone formation by osteoblasts. Osteoblasts not only play a central role in bone formation by synthesizing multiple bone matrix proteins, but regulate osteoclast maturation by soluble factors and cognate interaction, resulting in bone resorption. Osteoclast maturation requires stimulation by RANKL expressed on osteoblasts, and the cognate interaction is mediated by firm adhesion via ICAM-1. During the processes, pro-inflammatory cytokines such as IL-1 and TNF-alpha, cause an imbalance in bone metabolism, by favoring bone resorption via the induction of RANKL and ICAM-1 on osteoblasts. These inflammatory signals originate from the immune system, the largest source of cell-derived regulatory signals, and such immunological signals to the bone are transmitted primarily via osteoblasts to induce osteoclast maturation, resulting in secondary osteoporosis. Actually, such phenomena mainly occur at the interface between proliferating synovium and bone tissue in rheumatoid arthritis (RA). Thus, therapeutic strategies for these conditions, an anti-TNF-alpha antibody and an IL-1 receptor antagonist, effective for treating RA disease activity, also reduce secondary osteoporosis and joint destruction. Based on an improved understanding of immune signals, investigation of the suppression of cell functions may lead to improved understanding and better treatment of diseases of bone metabolism and osteoporosis.
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            An introduction to the pathophysiology of osteoarthritis.

            Jill Poole (1999)
            Osteoarthritis involves the degeneration of articular cartilage together with changes in subchondral bone and limited intra-articular inflammation. In this chapter these changes are reviewed at the tissue, cell and molecular levels to reveal the complexity of a process which involves multiple changes in joint structure and turnover.
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              Receptor activator of NF-kappaB ligand induces the expression of carbonic anhydrase II, cathepsin K, and matrix metalloproteinase-9 in osteoclast precursor RAW264.7 cells.

              Osamu Takeichi, Masao Maeno, M Makimura … (2007)
              Interleukin-1 (IL-1) is a proinflammatory cytokine that is a potent stimulator of bone resorption and an inhibitor of bone formation, whereas macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-kappaB (RANK) ligand (RANKL) are essential and sufficient for osteoclast differentiation. Recently, we showed that IL-1alpha affects mineralized nodule formation in vitro and halts bone matrix turnover. We also showed that IL-1alpha stimulates osteoclast formation via the interaction of RANKL with RANK by increasing M-CSF and prostaglandin E(2) and decreasing osteoprotegerin. Here, we examined the effects of IL-1alpha or RANKL and/or M-CSF in the presence of IL-1alpha on the expression of carbonic anhydrase II (CAII), cathepsin K, matrix metalloproteinase-9 (MMP-9), RANK, M-CSF receptor (c-fms), and c-fos transcription factor using RAW264.7 cells as osteoclast precursors. Cells were cultured for up to 14 days in 0 or 100 U/ml IL-1alpha and either 50 ng/ml RANKL, 10 ng/ml M-CSF, or 50 ng/ml RANKL+10 ng/ml M-CSF in the presence of 100 U/ml IL-1alpha. The formation of osteoclast-like cells was estimated using tartrate-resistant acid phosphatase staining. Expression of the genes coding for the six proteins of interest was determined using real-time PCR, and the expression of the three enzymes was examined using Western blotting or ELISA. In the presence of IL-1alpha, expression of CAII, cathepsin K, and MMP-9 was markedly increased in cells cultured with RANKL or M-CSF+RANKL, whereas expression was difficult to detect in cells cultured with IL-1alpha alone and M-CSF. RANK and c-fos expression was also increased in cells cultured with RANKL or M-CSF+RANKL in the presence of IL-1alpha, whereas c-fms expression did not change. These results indicate that the expression of CAII, cathepsin K, and MMP-9 in RAW264.7 cells is not induced by M-CSF, but by RANKL in the presence of IL-1alpha.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date (Print): 2009
                Publication date (Electronic): 24 February 2010
                Volume: 2009
                Electronic Location Identifier: 308596
                Affiliations
                1Nihon University Graduate School of Dentistry, Tokyo 101-8310, Japan
                2Department of Fixed Prosthodontics, Nihon University School of Dentistry, 1-8-13, Kanda Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan
                3Division of Advanced Dental Treatment, Dental Research Center, Nihon University School of Dentistry, Tokyo 101-8310, Japan
                4Department of Oral Health Sciences, Nihon University School of Dentistry, Tokyo 101-8310, Japan
                5Department of Biochemistry, Nihon University School of Dentistry, Tokyo 101-8310, Japan
                6Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, Tokyo 101-8310, Japan
                Author notes

                Recommended by Muzamil Ahmad

                Article
                DOI: 10.1155/2009/308596
                PMC ID: 2829618
                PubMed ID: 20204061
                SO-VID: 903ecbe0-0760-4afb-a21c-fa1e32ed9ee9
                Copyright © Copyright © 2009 Yusuke Watanabe et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 25 June 2009
                Date revision received : 28 August 2009
                Date accepted : 1 December 2009
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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