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Abstract Number: 958

Tumor Necrosis Factor-α Induces Production of Eotaxin-1/CCL11 from Fibroblast-like Synoviocyte in Rheumatoid Arthritis

Kuninobu Wakabayashi, Takeo Isozaki, Airi Nishimi, Shinichiro Nishimi, Sho Ishii, Takahiro Tokunaga, Hidekazu Furuya and Tsuyoshi Kasama, Div of Rheumatology, Showa University School of Med, Shinagawa-ku Tokyo, Japan

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: Chemokine Receptors, chemokines, cytokines and rheumatoid arthritis (RA)

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Session Information

Date: Monday, November 6, 2017

Session Title: Cytokines, Mediators, Cell-Cell Adhesion, Cell Trafficking and Angiogenesis Poster II: Mesenchymal Cells Do React - But How?

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: Chemokine C-C motif ligand 11 (CCL11) also known as eotaxin-1 is a member of the CC chemokine family, which acts as a major chemoattractant of eosinophils and a stimulator of basophils. Eotaxin-1/CCL11 is produced by lymphocytes, eosinophils and monocytes/macrophages and interacts with C-C chemokine receptor 3 (CCR3). CCR3 is associated with numerous inflammatory conditions and a recent study has also suggested expression of CCR3 on fibroblast-like synoviocyte (FLS) in rheumatoid arthritis (RA). In this study, we investigate the expression and the role of eotaxin-1/CCL11 and CCR3 in RA.

Methods: The levels of eotaxin-1/CCL11 were determined in serum from healthy control (HC) and the patients with RA using enzyme-linked immunosorbent assay (ELISA). We also measured the levels of eotaxin-1/CCL11 and tumor necrosis factor α (TNF-α) in synovial fluids (SFs) from the patients with RA and osteoarthritis (OA) using ELISA. To investigate the expression of eotaxin-1/CCL11 on RA FLS, cells were left unstimulated or were stimulated for 12-, 24- and 48-hours with 50 ng/mL of TNF-α. After stimulation, the protein expression levels of eotaxin-1/CCL11 in TNF-α treated RA FLS conditioned medium were measured by ELISA and the messenger RNA (mRNA) expression of eotaxin-1/CCL11 and CCR3 in RA FLS were measured by quantitative polymerase chain reaction (qPCR) analysis. The expression of eotaxin-1/CCL11 on RA FLS was demonstrated by immunohistochemistry.

Results: The levels of eotaxin-1/CCL11 in the serum from RA were higher than those in the serum from HC [mean ± SEM; 76 ± 6 pg/mL (n=48) and 52 ± 9 pg/mL (n=31), p<0.05, respectively]. The levels of eotaxin-1/CCL11 in SFs from the patients with RA were higher than those in SFs from the patients with OA [mean ± SEM; 61 ± 24 pg/mL (n=43) and 9 ± 2 pg/mL (n=20), p<0.05, respectively] and were positively correlated with the levels of TNF-α (r=0.35, p<0.05). The expression of eotaxin-1/CCL11 mRNA and the secretion of eotaxin-1/CCL11 in RA FLS were time-dependently increased by TNF-α stimulation following 12-, 24- and 48-hours (p<0.05). The expression of CCR3 mRNA was also induced time-dependently by TNF-α stimulation (p<0.05). Furthermore, it was observed that the eotaxin-1/CCL11 mRNA expression was positively correlated with the CCR3 mRNA expression (r=0.89, p <0.01). In addition, we confirmed that the expression of eotaxin-1/CCL11 on RA FLS was increased with TNF-α stimulation using immunohistochemistry.

Conclusion: These data indicate that TNF-α induced production of eotaxin-1/CCL11 from RA FLS, suggesting that eotaxin-1/CCL11 and CCR3 may play an important role of inflammation in RA.


Disclosure: K. Wakabayashi, None; T. Isozaki, None; A. Nishimi, None; S. Nishimi, None; S. Ishii, None; T. Tokunaga, None; H. Furuya, None; T. Kasama, None.

To cite this abstract in AMA style:

Wakabayashi K, Isozaki T, Nishimi A, Nishimi S, Ishii S, Tokunaga T, Furuya H, Kasama T. Tumor Necrosis Factor-α Induces Production of Eotaxin-1/CCL11 from Fibroblast-like Synoviocyte in Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/tumor-necrosis-factor-%ce%b1-induces-production-of-eotaxin-1ccl11-from-fibroblast-like-synoviocyte-in-rheumatoid-arthritis/. Accessed January 27, 2023.
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