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Abstract Number: 2079

Anti-Interleukin-6 Receptor Antibody Improves Systemic Osteoporosis in a Mice Model of Glucose-6-Phosphate Isomerase-Induced Arthritis

Hiroto Yoshida1, Miho Suzuki1, Misato Hashizume1, Keisuke Tanaka2, Masashi Shiina2, Isao Matsumoto3, Takayuki Sumida3 and Yoshihiro Matsumoto2, 1Product Research Department, Chugai Pharmaceutical Co., Ltd., Gotemba, Japan, 2Product Research Department, Chugai Pharmaceutical Co., Ltd., Gotemba, Shizuoka, Japan, 3Division of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Japan

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: animal models and tumor necrosis factor (TNF), interleukins (IL), osteoporosis, rheumatoid arthritis

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Session Information

Title: Rheumatoid Arthritis: Animal Models

Session Type: Abstract Submissions (ACR)

Background/Purpose: Patients with rheumatoid arthritis (RA) have a high risk of osteoporosis and osteoporotic fracture. In addition to the primary risk factors for osteoporosis, osteoporosis in RA is characterized by a complexity of other risk factors, including inflammation, immobilization, and use of corticosteroids. Anti-human interleukin-6 (IL-6) receptor antibody and various TNF inhibitors have an excellent therapeutic effect on RA symptoms, such as inflammation, pain, and swelling of joints. However, it is not fully understood whether inhibition of IL-6 and TNF-α can improve osteoporosis in patients with RA. Here, we investigated the interaction between proinflammatory cytokines and bone loss, using glucose-6-phosphate isomerase (GPI)-induced arthritis.

Methods: GPI-induced arthritis in DBA/1J mice was triggered by intradermal injection of recombinant GPI. Mice were injected once with anti-mouse IL-6 receptor antibody (MR16-1) intraperitoneally 5 days after immunization. On the other hand, TNF receptor-Fc (TNFR-Fc) was given intraperitoneally 3 times per week from the 5th day of immunization. The femurs of mice were harvested at various time points and the lumbar spine was excised at day 35. The trabecular bone volume (BV/TV) of the femurs and the lumbar spine was analyzed by using micro-computed tomography (μCT).

Results: First, we examined the severity of bone loss in GPI-induced arthritis. In immunized mice, BV/TV of femurs had significantly declined by 32.5% on day 7 (beginning of swelling) and by 61.5% on day 14 (peak of swelling) compared with non-immunized mice. Thereafter, as the swelling decreased, BV/TV of femurs in immunized mice was gradually recovered to 61.0% of non-immunized mice by day 35. Because arthritis significantly decreased the bone volume of femurs in mice, we next examined the involvement of IL-6 and TNF-α in bone loss in GPI-induced arthritis. Both MR16-1 and TNFR-Fc significantly suppressed the development of arthritis compared with untreated immunized mice. In MR16-1-treated mice, BV/TV of femurs and lumbar spine on day 35 was significantly increased to 1.3-fold and 1.2-fold that in untreated arthritic mice. On the other hand, TNFR-Fc increased the bone volume of femurs to 1.2-fold, but it did not affect that of the lumbar spine.

Conclusion: We demonstrated that IL-6 and TNF-α play a crucial role in bone loss of femurs caused by inflammatory arthritis in mice. However, in the lumbar spine, IL-6 is involved in bone loss but TNF-α is not. This suggests that blockade of IL-6 would have a beneficial effect on systemic osteoporosis in RA patients.


Disclosure:

H. Yoshida,
None;

M. Suzuki,
None;

M. Hashizume,
None;

K. Tanaka,
None;

M. Shiina,
None;

I. Matsumoto,
None;

T. Sumida,
None;

Y. Matsumoto,
None.

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