Disease relevance of Arthritis, Experimental

• Administration of bisindolylmaleimide VIII to rats during autoantigen stimulation prevented the development of symptoms of T cell-mediated autoimmune diseases in two models, the Lewis rat model of experimental allergic encephalitis and the Lewis adjuvant arthritis model [1].
• Oral administration of 13-cis-retinoic acid (40 or 160 milligrams per kilogram of body weight daily) significantly reduced the inflammation associated with developing and established adjuvant arthritis, an experimentally induced arthritis in rats that resembles human rheumatoid arthritis [2].
• To study the role of IRF-1 in autoimmunity, we investigated type II collagen-induced arthritis (CIA), and experimental allergic encephalomyelitis (EAE), in mice lacking IRF-1 [3].
• The disease is a chronic proliferative synovitis, resembling adjuvant arthritis in rats and rheumatoid arthritis in humans [4].
• We tested this hypothesis by using type II collagen-specific (CII-specific) CD4(+) T hybridomas or primary CD4(+) T cells after gene transfer, as vehicles to deliver an immunoregulatory protein for the treatment of collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis (RA) [5].

High impact information on Arthritis, Experimental

• We show that expression of SLC22A4 is specific to hematological and immunological tissues and that SLC22A4 is also highly expressed in the inflammatory joints of mice with collagen-induced arthritis [6].
• In addition, this peptide significantly reduced the severity of collagen-induced arthritis in mice by reducing levels of tumor necrosis factor-alpha and interleukin-1 beta, abrogating joint swelling and reducing destruction of bone and cartilage [7].
• We conclude that the suppression of collagen-induced arthritis was caused by an expansion of new CD11c(+)CD8(+) T cells, and that interferon-gamma produced by these cells suppresses antigen-specific CD4(+) T cells through an indoleamine 2,3-dioxygenase-dependent mechanism [8].
• Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand [9].
• Marked amelioration of established collagen-induced arthritis by treatment with antibodies to CD23 in vivo [10].

Chemical compound and disease context of Arthritis, Experimental

• Since the receptors for FGF-1 and PDGF are tyrosine kinases, we examined the expression of tyrosine phosphorylated proteins (phosphotyrosine, P-Tyr) in synovial tissues from patients with RA and osteoarthritis (OA), and rats with streptococcal cell wall (SCW) and adjuvant arthritis (AA) [11].
• The compounds were active against oxazolone dermatitis in mice and adjuvant arthritis in rats, models in which activated T lymphocytes are implicated [12].
• Effects of combination M40403 and dexamethasone therapy on joint disease in a rat model of collagen-induced arthritis [13].
• The hormone estriol increases during pregnancy and has been shown to ameliorate experimental autoimmune encephalomyelitis and collagen-induced arthritis [14].
• We established adjuvant arthritis in male and female Sherman strain rats and then studied external calcium balances and vitamin D metabolism during the period of acute active clinical, serologic, and pathologic arthritis and osteopenia and in the preclinical period [15].

Biological context of Arthritis, Experimental

• B10.Q (H-2q) mice congenic for the truncated T cell receptor (TCR) V beta a and V beta c haplotypes were derived to examine the influence of TCR V beta genomic deletions in murine collagen-induced arthritis (CIA) [16].
• We tested here if arthritic joint destruction was inhibited upon inactivation of the c-fos/AP-1 signal by administering short double-stranded AP-1 DNA oligonucleotides into mice with collagen-induced arthritis to compete for the binding of AP-1 in vivo at the promoter binding site [17].
• Plasmid encoding interleukin-4 in the amelioration of murine collagen-induced arthritis [18].
• Kinetics of bone protection by recombinant osteoprotegerin therapy in Lewis rats with adjuvant arthritis [19].
• OBJECTIVE: To investigate the effect of intermittent administration of human parathyroid hormone (PTH) on bone mineral density (BMD) and arthritis in rats with collagen-induced arthritis (CIA) [20].

Anatomical context of Arthritis, Experimental

• We, therefore, studied the in vivo expression of COX in synovia from patients with rheumatoid arthritis (RA) and osteoarthritis (OA), as well as joints of rats with streptococcal cell wall (SCW) and adjuvant arthritis [21].
• IL-18 enhances collagen-induced arthritis by recruiting neutrophils via TNF-alpha and leukotriene B4 [22].
• Genetically modified, coxsackie-Ad receptor-independent Ad5 vectors were studied for gene delivery in human RA FLS and synovium explants and murine collagen-induced arthritis [23].
• Gene transfer of a fibronectin peptide inhibits leukocyte recruitment and suppresses inflammation in mouse collagen-induced arthritis [24].
• OBJECTIVE: To investigate the therapeutic effects and possible mechanisms of action of constitutive expression of interferon-beta (IFNbeta) by syngeneic fibroblasts from DBA/1 mice in the collagen-induced arthritis (CIA) model [25].

Associations of Arthritis, Experimental with chemical compounds

• Inflammation and collagenase production in rats with adjuvant arthritis reduced with 13-cis-retinoic acid [2].
• Paradoxical effects of cyclosporin A on collagen arthritis in rats [26].
• Prostacyclin-IP signaling and prostaglandin E2-EP2/EP4 signaling both mediate joint inflammation in mouse collagen-induced arthritis [27].
• We have found that serum from rats with type II collagen-induced arthritis, when fractionated with 50% ammonium sulfate and concentrated, would transfer arthritis to nonimmunized recipients [28].
• Blood mononuclear cells from the majority of rats with adjuvant arthritis exhibited enhanced thymidine incorporation to homologous types I and II collagens, as well as to purified protein derivative of tuberculin [29].

Gene context of Arthritis, Experimental

• In a T-cell-dependent model of rat adjuvant arthritis characterized by severe joint inflammation, bone and cartilage destruction and crippling, blocking of OPGL through osteoprotegerin treatment at the onset of disease prevents bone and cartilage destruction but not inflammation [9].
• In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice [30].
• Interleukin 6 is required for the development of collagen-induced arthritis [31].
• Interleukin-10 expression and chemokine regulation during the evolution of murine type II collagen-induced arthritis [32].
• Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis [33].

Analytical, diagnostic and therapeutic context of Arthritis, Experimental

• The clinical severity in mice undergoing collagen-induced arthritis was significantly reduced after treatment with both IL-18 neutralizing agents compared to placebo treated mice [34].
• DNA vaccination with CD25 protects rats from adjuvant arthritis and induces an antiergotypic response [35].
• Here we investigate the effects of the tyrosine kinase inhibitor tyrphostin AG126 in two animal models of acute and chronic inflammation, carrageenan-induced pleurisy and collagen-induced arthritis [36].
• Gene therapy targeting the Tie2 function ameliorates collagen-induced arthritis and protects against bone destruction [37].
• The effect of anti-MIF antibody administration on murine passive collagen-induced arthritis (CIA) was also evaluated by histologic examination and reverse transcriptase-polymerase chain reaction [38].

References