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

Collagen-induced arthritis (CIA) was found to be useful as an animal model to investigate the mechanism by which rheumatoid arthritis is developed. We therefore studied variations of T and B lymphocytes in peripheral blood and bone marrow in order to ascertain the importance of T and B lymphocytes in the development of CIA. T lymphocyte, which is considered to be associated with the onset and deterioration of CIA, was not changed during the course of CIA, whereas B lymphocyte, which produces anti-type II collagen antibody regarded as an indispensable factor in CIA induction, was significantly decreased in peripheral blood and bone marrow at 10 days after the 2nd immunization when arthritis was able to be detected. In bone marrow, although two cell populations of Ly5/B220-positive cells were detected, only the cell population with lower fluorescence intensity was decreased transiently. These results suggest that B lymphocyte in both bone marrow and peripheral blood is intimately involved in the course of CIA.
 ...
PMID:Variation of lymphocytes in peripheral blood and bone marrow in collagen-induced arthritis. 800 25

Collagen-induced arthritis (CIA) in DBA-1 lac/J mice often has a low incidence, with gradual disease expression occurring over a broad time span (between days 35 and 70). The exact mechanisms underlying spontaneous expression are still poorly understood, although it is evident that some inflammatory cytokines like IL-1, tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta) are potent accelerators. We have investigated whether we could trigger collagen type II-driven inflammation by: (i) enhancing anti-collagen type II (CII) antibodies, or (ii) a non-related inflammatory process. Male DBA-1 lac/J mice were immunized with 100 micrograms bovine type II collagen in Freund's complete adjuvant (FCA), resulting in a low disease expression at day 28. Addition of anti-CII antibodies slightly enhanced the expression of CIA. Zymosan (3 mg), given intraperitoneally, induced consistent expression of CIA after 1 week, whereas a retarded onset was noted with higher dosages. Local injection of a low dose of Zymosan (60 micrograms) in the knee joint, clearly potentiated the expression of CIA at that particular site. Higher concentrations not only elicited prolonged CIA expression at the injection site, but also induced marked CIA in the draining ankle joint. In contrast, intra-articular injection of Zymosan in nonimmunized DBAs or methylated bovine serum albumin (mBSA)/FCA-immunized controls only induced transient joint inflammation. The nature of the highly erosive CIA was confirmed histologically, and could easily be discriminated from the reversible changes induced with Zymosan. Our data indicate that latent autoimmune reactions may come to expression at the moment of non-specific inflammation, even at a remote site.
 ...
PMID:Accelerated onset of collagen-induced arthritis by remote inflammation. 805 Jan 68

Collagen-induced arthritis is an arthritic disease that can be induced in rodents and primates. It is used widely as a model of disease processes and potential therapies. The immunology of collagen arthritis has some compelling parallels with human disease and these have been exploited recently in several novel ways to analyse the nature of autoreactivity against joint antigens and to test new therapies. Antibodies against lymphocyte surface markers, such as CD4, CD40L and MHC Class II, have been shown to suppress disease progression. Manipulation of cytokines, notably TNF-alpha, IL-1 and IL-2, has been extensively studied using the cytokines themselves, antibodies against cytokines and other antagonists with varied, but promising results. The search for antigen-specific immunosuppression has gained new impetus through manipulation of collagen arthritis by mucosal delivery of collagen to induce tolerance that suppresses disease. This review examines the salient features of collagen arthritis that are relevant to human disease and discusses the meaning and potential application of experimental therapies to the control of human arthritis.
 ...
PMID:Collagen arthritis--what can it teach us? 808 63

The importance of a collagen-binding adhesin in the pathogenesis of septic arthritis has been examined by comparing the virulence of two sets of Staphylococcus aureus mutants in an animal model. Collagen adhesin-negative mutant PH100 was constructed by replacing the chromosomal collagen adhesin gene (cna) in a clinical strain, Phillips, with an inactivated copy of the gene. Collagen adhesin-positive mutant S. aureus CYL574 was generated by introducing the cna gene into CYL316, a strain that normally lacks the cna gene. Biochemical, immunological, and functional analyses of the generated mutants and their respective parent strains showed that binding of 125I-labeled collagen, expression of an immunoreactive collagen adhesin, and bacterial adherence to cartilage were directly correlated with the presence of a functional cna gene. Greater than 70% of the mice injected with the Cna+ strains developed clinical signs of arthritis, whereas less than 27% of the animals injected with Cna- strains showed symptoms of disease. Furthermore, mice injected with the Cna+ strain Phillips had remarkably elevated levels of immunoglobulin G1 and interleukin-6 compared with mice injected with the Cna- mutant PH100. Taken together, these results demonstrate that collagen adhesin plays an important role in the pathogenesis of septic arthritis induced by S. aureus.
 ...
PMID:The Staphylococcus aureus collagen adhesin is a virulence determinant in experimental septic arthritis. 826 22

Total medial meniscectomy was performed in 12 adult merino sheep. Immediately after surgery, 8 animals received high-molecular-weight hyaluronan (HA) (1 mL, 10 mg/mL) and 4 were given sterile saline (1 mL) intraarticularly. Injections were given for 5 more weeks. In week 3 an exercise program, consisting of walking 24 km/wk, was initiated. This program was continued until the animals were killed at week 26 postmeniscectomy. At necropsy the lateral menisci were removed and divided into three concentric zones--inner, middle, and outer. Powdered aliquots of tissues from each zone were analyzed for collagen and hexuronate contents using colormetric methods. The glycosaminoglycans (GAGs)--chondroitin-O-sulfate (C-O-S), chondroitin-4-sulfate (C-4-S), chondroitin-6-sulfate (C-6-S), and dermatan sulfate (DS)--were determined using a high-performance liquid chromatography method. The lateral menisci from the joints of animals injected with HA showed higher hexuronate and GAG levels than those of controls. This increase was mainly due to C-6-S, which had highest levels in the inner and middle meniscal zones. In addition, dermatan sulfate levels increased significantly in the middle and outer zones of the lateral menisci compared with the same zones of the meniscus from the saline-treated group. Collagen and C-O-S levels were not statistically different from those of controls. These data suggest that intraarticular administration of high-molecular-weight HA immediately after open total medial meniscectomy may help preserve the proteoglycans in the lateral meniscus remaining in the joint.
Semin Arthritis Rheum 1993 Jun
PMID:Effects of intraarticular hyaluronan on matrix changes induced in the lateral meniscus by total medial meniscectomy and exercise. 834 52

Collagen type II-induced arthritis (CIA) is generated in susceptible rodent strains by intradermal injections of homologous or heterologous native type II collagen in complete Freund's adjuvant. Symptoms of CIA are analogous to those of the human autoimmune disease, rheumatoid arthritis. CIA is a model system for T cell-mediated autoimmune disease. To study the T cell receptor (TCR) repertoire of bovine type II-specific T cells that may be involved in the pathogenesis of CIA in DBA/1Lac.J (H-2q) mice, 13 clonally distinct T cell hybridomas specific for bovine type II collagen have been established and the alpha and beta chains of their TCRs have been analyzed. These T cell hybridomas recognize epitopes that are shared by type II collagens from distinct species and not by type I collagens, and exhibit a highly restricted TCR-alpha/beta repertoire. The alpha chains of the TCRs employ three V alpha gene subfamilies (V alpha 11, V alpha 8, and V alpha 22) and four J alpha gene segments (J alpha 42, J alpha 24, J alpha 37, and J alpha 32). The V alpha 22 is a newly identified subfamily consisting of approximately four to six members, and exhibits a high degree of polymorphism among four mouse strains of distinct V alpha haplotypes. In addition, the beta chains of the TCRs employ three V beta gene subfamilies (V beta 8, V beta 1, and V beta 6), however the V beta 8.2 gene segment is preferentially utilized (58.3%). In contrast, the J beta gene segment usage is more heterogeneous. On the basis of the highly limited TCR-alpha/beta repertoire of the TCRs of the panel of bovine type II-specific T cell hybrid clones, a significant reduction (60%) of the incidence of arthritis in DBA/1Lac.J mice is accomplished by the use of anti-V beta 8.2 antibody therapy.
 ...
PMID:Characterization of the T cell receptor repertoire causing collagen arthritis in mice. 838 Nov 55

Collagen induced arthritis (CIA) is an animal model of inflammatory polyarthritis. Immunotherapy with the monoclonal antibody F23.1, which deletes V beta 8 bearing T cells, significantly decreased the incidence of CIA in mice. Treatment with the monoclonal antibody 466B5, to delete V beta 6 bearing T cells in combination with F23.1 was no more effective than F23.1 alone and the CIA incidence in 466B5 treated animals was not significantly different from controls. Thus, the V beta 8 family of T cell receptor is expressed on self-reactive T cells in the CIA model of B10.RIII mice injected with porcine type II collagen.
 ...
PMID:Prevention of collagen induced arthritis in mice by deletion of T cell receptor V beta 8 bearing T cells with monoclonal antibodies. 842 55

Collagen-induced arthritis is an experimental model for rheumatoid arthritis which can be elicited in susceptible strains of rats by intradermal injection of native type II collagen. In order to investigate whether bacterial flora may alter the pathogenic response to type II collagen, we have immunized germ-free (GF) male rats from either highly resistant Fisher (F344) or highly susceptible Dark Agouti (DA) strains. The disease was markedly enhanced in GF DA as compared to conventional (CV) DA rats. The humoral response was also stronger in GF rats of both strains. Neither GF nor CV F344 developed arthritis, although GF F344 exhibited later inflammation of the tail. These data support a suppressive influence of bacterial flora on collagen-induced arthritis.
 ...
PMID:Influence of the bacterial flora on collagen-induced arthritis in susceptible and resistant strains of rats. 845 1

Collagen-induced arthritis (CIA) is an (autoimmune) joint disease readily elicited in DBA/1 mice by immunization with type II collagen (CII) emulsified with complete Freund's adjuvant. It is a destructive arthritis involving about 50% of the limbs and occurs with an incidence of 70% to 100%. In this study we evaluated the effect of mouse recombinant interleukin-12 (mrIL-12) on CIA. Administration of mrIL-12 at high doses (1 micrograms/mouse, daily) for 2 or 3 weeks delayed the onset and reduced the incidence of CIA. Furthermore, the severity of CIA was much milder and in most cases restricted to single digits of the paws. Short-term administration of high doses of IL-12 exerted some, but less pronounced, disease-suppressing effect. In contrast, 10-fold lower doses of IL-12 given during the first 3 weeks, or high doses of IL-12 administered therapeutically proved to be ineffective. Only those regimens of IL-12 treatment that ameliorated CIA were associated with a down-regulation of the CII-specific antibody response. A strong inhibition of CII-specific IgG1 antibodies (10- to 20-fold) and a moderately (2- to 6-fold) suppressed IgG2b response was observed, whereas the level of CII-specific IgG2a antibodies remained high. Taken together, the results indicate that some initial events in the induction of CIA in DBA/1 mice injected with CII emulsified with CFA are suppressed by treatment with high doses of IL-12.
 ...
PMID:High doses of interleukin-12 inhibit the development of joint disease in DBA/1 mice immunized with type II collagen in complete Freund's adjuvant. 856 65

Collagen-induced arthritis is mediated by autoantibodies to type II collagen (CII). This experimental model has proven useful in determining the molecular and cellular mechanisms responsible for autoimmune arthritis. We have shown that polyarthritis can be transferred to normal mice by administering combinations of three or four complement-fixing monoclonal antibodies (mAbs) which recognize cross-reactive epitopes on the alpha 1(II)-CB11 region of chick and mouse CII. Currently, the light- and heavy-chain variable-region structures on a panel of alpha 1 (II)-CB11-specific mAbs that cross-react with chick and mouse CII, or react solely with chick CII, have been analyzed. The results indicate biased usage of VK19 and VK21 families of light-chain variable-region genes but random VH gene usage. Interestingly, two mAbs derived from different mice recognized identical epitopes on mouse CII and had nearly identical light- and heavy-chain variable-region structure including junctionally derived sequence.
 ...
PMID:Variable-region gene family usage for type II collagen autoantibodies in arthritis-susceptible DBA/1 mice. 860 2


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>