The Role of Monocyte Chemoattractant Protein‐1 (Mcp‐1) in the Pathogenesis of Collagen‐induced Arthritis in Rats

Ogata, Hiromi; TAKEYA, Motohiro; Yoshimura, Teizo; Takagi, Katsumasa; Takahashi, Kiyoshi

doi:10.1002/(sici)1096-9896(199705)182:1<106::aid-path816>3.3.co;2-1

Cited by 25 publications

(32 citation statements)

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“…The role of MCP-1 in an inflamed RA joint may be the recruitment of mononuclear phagocytes. And in fact, the effectiveness of anti-MCP-1 antibody treatments against arthritis development has been reported in some arthritis models [32,33]. In our study, IL-1β and MCP-1 mRNA expression were markedly increased in the arthritis group compared to the control group.…”

Section: Discussionsupporting

confidence: 49%

Inhalation of Carbon Monoxide Ameliorates Collagen-induced Arthritis in Mice and Regulates the Articular Expression of IL-1β and MCP-1

et al. 2009

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Carbon monoxide (CO), long considered a toxic gas, has recently been shown to mediate anti-inflammatory effects in various animal models. The aim of this study was to investigate whether the inhalation of CO ameliorated collagen-induced arthritis (CIA) in mice. CIA was induced in female DBA/1 mice by the injection of an anti-type II collagen antibody and lipopolysaccharide. The CO treatment group was exposed to CO gas at a concentration of 200 ppm in a closed cage starting on the day of the injection with an anti-type II collagen antibody and throughout the remaining study period. The clinical arthritis scores was examined daily for swelling of the paws as a sign of arthritis. For histopathology, the sections of the hind legs were evaluated by hematoxylin-eosin staining. Moreover, we evaluated the expression of interleukin (IL)-1beta and monocyte chemoattractant protein-1 (MCP-1) mRNA in the hind paws. Both clinical arthritis scores as well as histological findings of joint inflammation were significantly reduced in mice treated with CO gas inhalation compared to untreated mice. Further, CO significantly inhibited the increased expression of IL-1beta and MCP-1 mRNA in paws at day 3 after the induction of arthritis. In conclusion, the inhalation of CO protected mice from the synovial inflammation of CIA. Based on these data, the beneficial effects of CO in murine RA model may be attributed to its anti-inflammatory properties.

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Section: Discussionsupporting

confidence: 49%

Inhalation of Carbon Monoxide Ameliorates Collagen-induced Arthritis in Mice and Regulates the Articular Expression of IL-1β and MCP-1

et al. 2009

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“…In the present study, we con®rm the increased production of MCP-1 and RANTES in rats with adjuvantinduced arthritis, in congruence with previous reports [15,16,17,18] and show that their enhanced production as well as the progression of arthritis are suppressed by treatment with KE-298. We also demonstrate that KE-298 suppresses MCP-1 and RANTES production by IL1b-stimulated RA synoviocytes, although MIP-1a in the supernatant of these synoviocytes was not reduced during treatment with KE-298 (data not shown).…”

Section: Discussionsupporting

confidence: 93%

“…Furthermore, excessive production of MCP-1 and RANTES by synoviocytes has been demonstrated in RA [10,11,12,13,14]. Both MCP-1 and RANTES have also been suggested to play important roles in the pathogenesis of arthritis in animal models including adjuvant-induced arthritis in rats, and treatment with an antagonist of these chemokines has signi®cantly suppressed the progression of arthritis in RA animal models [15,16,17,18].…”

Section: Introductionmentioning

confidence: 99%

The new antirheumatic drug KE-298 suppresses monocyte chemoattractant protein (MCP)-1 and RANTES production in rats with adjuvant-induced arthritis and in IL-1?-stimulated synoviocytes of patients with rheumatoid arthritis

Yamashita

Higaki

2001

Rheumatology International

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We analyzed the effects of the new antirheumatic drug KE-298 on monocyte chemoattractant protein (MCP)-1 and regulated on activation normal T-cell expressed and secreted (RANTES) production in rats with adjuvant-induced arthritis and in interleukin (IL)-1beta-stimulated rheumatoid arthritis (RA) synoviocytes. In rats with adjuvant-induced arthritis, the enhanced production of MCP-1 and RANTES and the development of arthritis were suppressed by oral treatment with 100 mg/kg per day of KE-298 for 18 days. Furthermore, KE-298 (10-100 microg/ml) suppressed MCP-1 and RANTES production by IL-1beta-stimulated RA synoviocytes through inhibition of NF-kappaB and AP-1 activation. These results suggest that the inhibitory effect of KE-298 on MCP-1 and RANTES production might partly explain its efficacy in rats with adjuvant-induced arthritis and in patients with RA.

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“…In AIA, anti-TNF␣ antibody treatment improved clinical scores and decreased leukocyte infiltration into the synovium (32). Both anti-MIP-1␣ and anti-MCP-1 antibodies have been tried successfully in CIA (4,49,55). In our recent study, an antibody to ENA-78 administered prior to the onset of AIA could prevent the development of arthritis.…”

Section: Discussionmentioning

confidence: 91%

Temporal expression of inflammatory cytokines and chemokines in rat adjuvant‐induced arthritis

Szekanecz

Halloran

Volin

et al. 2000

Arthritis & Rheumatism

159

120

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Objective. To examine cytokine and chemokine production during the evolution of rat adjuvant-induced arthritis (AIA), a model of rheumatoid arthritis. Methods. Clinical and laboratory assessment of the course of AIA was performed over a 47-day period. Levels of the cytokines tumor necrosis factor (TNF), interleukin-1 (IL-1), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1 (MIP-1) and JE, the murine homolog of monocyte chemoattractant protein 1, were determined by enzyme-linked immunosorbent assay in the sera and joints of AIA and control rats. Synovia from AIA rats were (immuno)histochemically analyzed. Results of cytokine and chemokine measurements were correlated with clinical and laboratory markers of inflammation and histology. Results. Early (before day 14 post adjuvant injection) and later phases of AIA could be distinguished. Cytokine and chemokine production was increased in AIA versus control rats. The production of TNF, IL-1, MIP-1, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of IL-6 and JE was elevated in the late phase of AIA. Cytokine and chemokine levels were correlated with the clinical symptoms of arthritis and blood neutrophil counts. Joint levels of IL-1 showed correlation with synovial lining proliferation and neutrophil ingress into AIA synovium. Conclusion. Cytokines and chemokines are involved in the clinical, laboratory, and histologic changes underlying AIA. The production of these mediators may be temporally and spatially regulated. These findings may be important for the optimal timing of cytokine and chemokine targeting.

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The Role of Monocyte Chemoattractant Protein‐1 (Mcp‐1) in the Pathogenesis of Collagen‐induced Arthritis in Rats

Cited by 25 publications

References 0 publications

Inhalation of Carbon Monoxide Ameliorates Collagen-induced Arthritis in Mice and Regulates the Articular Expression of IL-1β and MCP-1

Inhalation of Carbon Monoxide Ameliorates Collagen-induced Arthritis in Mice and Regulates the Articular Expression of IL-1β and MCP-1

The new antirheumatic drug KE-298 suppresses monocyte chemoattractant protein (MCP)-1 and RANTES production in rats with adjuvant-induced arthritis and in IL-1?-stimulated synoviocytes of patients with rheumatoid arthritis

Temporal expression of inflammatory cytokines and chemokines in rat adjuvant‐induced arthritis

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