Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapeutic action of lobenzarit disodium (CCA) on the function of endothelial cells (EC) isolated from human umbilical cord veins was investigated. CCA suppressed 3H-thymidine incorporation into EC in a dose-dependent manner. Significant inhibition was detected at a concentration of 50 micrograms/ml. The expression of HLA-DR antigen on the surface of EC was increased when EC were cultured with recombinant interferon-gamma (rIFN gamma). Treatment of EC with either IFN gamma or interleukin-1 enhanced the adhesion of T cells to EC. The kinetics of HLA-DR antigen expression by EC cultured with IFN gamma was different from the kinetics of T cell-EC adhesion, however. Neither anti-HLA-DR nor anti-HLA-ABC monoclonal antibody inhibited T cell binding to EC monolayers. CCA suppressed the expression of HLA-DR antigen by EC cultured with rIFN gamma. In an EC monolayer adhesion assay, CCA also inhibited T cell adhesion to EC in the presence of either IFN gamma or interleukin-1. Significant inhibition was observed at a CCA concentration of 10 micrograms/ml, a level that is easily attainable in serum. These results suggest that CCA may suppress rheumatoid synovitis by reducing the angiogenesis and emigration of chronic inflammatory cells from the blood into the synovium.
Arthritis Rheum 1991 Mar
PMID:Effects of lobenzarit disodium on human endothelial cells. Lobenzarit disodium inhibits proliferative response, HLA-DR antigen expression, and T cell adherence toward endothelial cells. 190 Jun 89

The effects of anti-rheumatic drugs (lobenzarit (CCA); 10 and 50mg/kg, cyclophosphamide (CP); 5 mg/kg and dexamethasone (DM); 0.25mg/kg) were evaluated immunologically and histopathologically on DBA/1J mice that develop polyarthritis after immunization by the intradermal injection of type II collagen. Serum anti-type II collagen IgG levels in the groups treated with CP and DM were significantly suppressed to 1/2 and 1/10 as compared to those of the positive control group, respectively. Those of both groups treated with CCA were not different from those of the positive control group. Histopathological examination revealed that treatment with CP and DM markedly reduced or suppressed inflammatory changes and resulted in low incidence of arthritis. From the standpoint mentioned above, treatment with anti-rheumatic drugs suppressed the development of arthritis in this model, and we could confirm that this model was useful for evaluation of the effect of anti-rheumatic drugs.
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PMID:Pathological evaluation of anti-rheumatic drugs on type II collagen-induced arthritis in DBA/1J mouse. 200 40

CCA(N-(2-carboxyphenyl)-4-chloroanthranilic acid disodium salt is a new synthetic compound which structurally resembles mefenamic acid. CCA induces inhibition of the adjuvant arthritis in rats and has been reported as activator of suppressor T lymphocytes. These findings stimulated to us to elucidate whether or not CCA possesses inhibitory effects on immunoglobulin E (IgE) production, an immunological system in which T suppressor cells play a cardinal role. Mice F1 (BALB/c x C57BL/6J) and C3H/A were immunized using the procedure of several s.c. injections with low dose of ovalbumin and aluminium hydroxide gel. CCA (5 mg/kg and 50 mg/kg) was administered to mice several weeks by oral route. The titers of IgE were compared in controls and treated animals using the method of passive cutaneous anaphylaxis (PCA) in rats. At a dose of 5 mg/kg CCA reduced partially the titers of IgE in treated animals with respect to controls and at a dose of 50 mg/kg this inhibition was more pronounced. These results support a potential usefulness of CCA in bronchial asthma and other immediate type allergic disorders.
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PMID:The immunomodulatory effect of CCA (N-(2-carboxyphenyl)-4-chloroanthranilic acid disodium salt) on IgG antibody response in mice immunized with ovalbumin. 251 12

In vitro effects of CCA, an anti-arthritis agent, were studied upon autologous mixed lymphocyte reaction (AMLR), lymphocyte mitogenesis, IL 1 and IL 2 production, immunoglobulin production and gamma-interferon (IFN) production. CCA at 50 micrograms/ml, which was not toxic to cells, blocked AMLR, IL 1 production and immunoglobulin production (IgM and IgG) significantly, while CCA at the same dose did not affect IL 2 production and lymphocyte mitogenic responses to Staphylococcus aureus Cowan I(SAC) and pokeweed mitogen(PWM). CCA at both 20 ng/ml and 20 micrograms/ml induced human gamma/IFN. Addition of IL 1 and/or IL 2 reversed inhibitory effect of CCA on AMLR. These data suggest that CCA exerts its actions by mainly affecting T cells and monocytes and can be used as an immunomodulator.
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PMID:Immunopharmacological study of CCA (Lobenzarit disodium), an anti-arthritis agent--I. Abrogation of IL 1 secretion by LPS-stimulated human monocytes and induction of gamma-interferon production with CCA. 308 53

A newly synthesized agent, disodium 4-chloro-2,2'-iminodibenzoate (CCA; Lobenzarit disodium), which prevents the development of autoimmune disease in B/W mice, and inhibits adjuvant arthritis in rats, was investigated to clarify its mode of action in B/W mice. CCA protected against the age-related decline of the suppressor T cell activity which played an important role in the regulation of both humoral and cell-mediated immunity. CCA also decreased the production of naturally occurring thymocytotoxic autoantibody (NTA) preferentially cytotoxic against the thymocytes and suppressor T cells, and inhibited both the antibody production to double-stranded DNA and the appearance of ANA in B/W mice.
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PMID:The effect of CCA (Lobenzarit disodium) on the suppressor T cell function and the production of autoantibodies in New Zealand black and New Zealand white F1 mice. 622 13

Lobenzarit disodium (CCA) has been reported to have an inhibitory effect on the development of adjuvant arthritis (AA) in rats. Earlier studies have suggested that the therapeutic effect of CCA might be based on its immunoregulatory activity, although the precise mechanisms of action are unclear. In this paper, possible involvement of thymus-derived lymphocytes in the suppression of AA was studied. It was found that CCA failed to inhibit the development of AA in rats whose T lymphocytes were depleted by the injection of rabbit antithymocyte serum (ATS), whereas the same schedule of treatment with CCA significantly suppressed AA developed in control rats which were injected with normal rabbit serum. In addition, adult thymectomy abrogated the antiarthritic effect of CCA. These data suggest the possibility that the therapeutic effect of CCA in AA might be mediated by ATS-sensitive, short-lived, thymus-derived lymphocytes.
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PMID:A novel antiarthritic agent, CCA (lobenzarit disodium), and the role of thymus-derived lymphocytes in the inhibition of rat adjuvant arthritis. 660 46

A single dose of either cyclosporin-A (CsA) or lobenzarit (CCA) given with an arthrogenic adjuvant completely prevented expression of experimental adjuvant arthritis in rats. The aim of this study was to understand how these drugs prevented the arthritis expression by studying the popliteal lymph nodes draining the arthritic joints at various times after adjuvant injection. Neither drug affected the proliferation in popliteal lymph nodes at the time arthritis was normally expressed, however, there was a marked change in the types of cells present. Immunofluorescence assays showed a reduction in the proportion of CD4+ cells, while the proportion of B-lymphocytes was almost doubled. This coincided with a marked elevation in the ability of these cells to produce interleukin (IL)-6. At the same time production of other cytokines (IL-2, tumour necrosis factor (TNF) and interferon (IFN)-gamma) was not greatly affected. However, one day after adjuvant injection IL-2 and IFN-gamma production was reduced. In vitro experiments showed that IL-6 production by lymphoid cells was relatively unaffected by CsA and CCA but IL-2, TNF and IFN-gamma were suppressed by CsA. The results indicate that CsA and CCA may modify the response to the arthritic adjuvant by specifically inhibiting IL-2, TNF and IFN-gamma production at the time of adjuvant injection. The lack of inhibition of IL-6 by these drugs reveals it may not play a key role in the initiation of this model of chronic inflammation.
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PMID:Complete prevention of the clinical expression of adjuvant-induced arthritis in rats by cyclosporin-A and lobenzarit: the regulation of lymph node cell populations and cytokine production. 874 Oct 4

An experimental study was performed to investigate the influence of chronic inflammation in peripheral target tissue on recovery of the sciatic nerve after crush injury. Thirty-four male Wistar rats, weighing 300-370 g were used. The sciatic nerve was crushed unilaterally with an aneurysm clip (250 gf; holding force; 5 min). One week before the operation, chronic inflammation, localized in the tibiotarsal joint of one hind limb, was produced by the intraarticular injection of complete Freund's adjuvant. The animals were divided into five groups, as follows: CIA (crush injury with ipsilateral arthritis), CCA (crush injury with contralateral arthritis), C (crush injury without arthritis), A (sham operation and ipsilateral arthritis), and S (sham operation without arthritis). Specimens for histological examination were taken from the nerve at a site 5 mm distal to the crush injury 4 weeks postoperatively. Histological study showed that the diameters of the axons in group CIA were significantly smaller than those in group CCA and those in group C. No significant differences were observed between group CCA and group C. In conclusion, peripheral nerve recovery after crush injury was suppressed by chronic inflammation in peripheral target tissue.
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PMID:Influence of chronic inflammation in peripheral target tissue on recovery of crushed nerve injury. 1184 51