Nurse-like cells from patients with rheumatoid arthritis support the survival of osteoclast precursors via macrophage colony-stimulating factor production
✍ Scribed by Hideki Tsuboi; Nobuyuki Udagawa; Jun Hashimoto; Hideki Yoshikawa; Naoyuki Takahashi; Takahiro Ochi
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 280 KB
- Volume
- 52
- Category
- Article
- ISSN
- 0004-3591
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✦ Synopsis
Abstract
Objective
To elucidate the role of nurse‐like cells (NLCs) obtained from rheumatoid arthritis (RA) patients in bone loss during progressive synovial expansion.
Methods
CD14+ monocytes were cocultured with NLCs for 4 weeks and collected as NLC‐supported CD14+ (NCD14+) monocytes. To determine their ability to differentiate into osteoclasts, NCD14+ monocytes were further cultured with macrophage colony‐stimulating factor (M‐CSF) together with RANKL or tumor necrosis factor α (TNFα). NCD14+ monocytes were also cocultured with SaOS‐4/3 cells, which were shown to support osteoclastogenesis in response to parathyroid hormone (PTH). CD14+ monocytes were cocultured with SaOS‐4/3 cells to elucidate how SaOS‐4/3 cells and NLCs supported CD14+ monocytes for a long period. Synovial expansion adjacent to bone in RA patients was examined immunohistochemically to detect osteoclast precursors such as NCD14+ monocytes.
Results
NLCs supported the survival of CD14+ monocytes for 4 weeks. NCD14+ as well as CD14+ monocytes differentiated into osteoclasts in the presence of M‐CSF together with RANKL or TNFα. NCD14+ monocytes also differentiated into osteoclasts in PTH‐treated cocultures with SaOS‐4/3 cells. SaOS‐4/3 cells supported the survival of CD14+ monocytes for 4 weeks in the presence, but not absence, of PTH. Treatment of SaOS‐4/3 cells with PTH up‐regulated the expression of M‐CSF messenger RNA. Neutralizing antibodies against M‐CSF inhibited the NLC‐supported survival of CD14+ monocytes. CD68+ monocytes and M‐CSF+ fibroblast‐like synoviocytes were colocalized in regions adjacent to the destroyed bone of RA patients.
Conclusion
Our findings suggest that NLCs are involved in RA‐induced bone destruction by maintaining osteoclast precursors via production of M‐CSF.