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)

We recently observed that specific antibodies to type II collagen do not bind in appreciable amounts to the intact surface of articular cartilage, whereas antibodies to the minor collagen types V, VI, and IX do. These results suggest that the outermost cartilage surface layer prevented interaction of the antibodies with the major collagen type in articular cartilage. The present studies were designed to investigate the pathogenic mechanisms involved in the disruption of the cartilage surface layer in inflammatory arthritis. Articular cartilage obtained from rabbits undergoing acute antigen-induced arthritis of 72 h duration showed a significant increase in binding of anti-type II antibody to cartilage surfaces compared with normal control cartilage (P less than 0.01). Augmentation of anti-type II binding was also observed upon in vitro incubation of bovine articular slices or intact rabbit patellar cartilage for 1 h with human polymorphonuclear neutrophils (PMN), PMN lysates, or purified human PMN elastase. This increase was not inhibited by sodium azide, nor was it enhanced by incubation of cartilage with the strong oxidant hypochlorous acid. Chondrocyte-mediated matrix proteoglycan degradation in cartilage explants cultured in the presence of cytokines failed to increase antibody binding appreciably. The augmentation in antibody binding seen with PMN lysates was inhibited by the nonspecific serine-esterase inhibitor PMSF, but not by the divalent metal chelator EDTA. The elastase-specific inhibitor AAPVCMK also inhibited most of the PMN-induced increase in antibody binding, whereas the cathepsin G-specific inhibitor GLPCMK was much less effective. Incubation of intact cartilage with purified human PMN elastase indicated that this serine esterase could account for the increase in anti-type II collagen antibody binding to intact cartilage surfaces. These studies suggest that in an inflammatory response, PMN-derived elastase degrades the outer layer of articular cartilage, exposing epitopes on type II collagen. They also help clarify the pathogenic mechanisms involved in early articular cartilage damage in inflammatory joint diseases.
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PMID:Mechanisms of disruption of the articular cartilage surface in inflammation. Neutrophil elastase increases availability of collagen type II epitopes for binding with antibody on the surface of articular cartilage. 170 82

Findings in 27 patients with typical skin lesions of urticarial vasculitis (UV) who were seen at a connective tissue disease clinic over a 5-year period (1986 to 1990) are reviewed. The majority suffered from systemic lupus erythematosus (SLE) or from "lupus-like" disease (18 patients), 1 from "mixed" connective tissue disease (MCTD), and 5 from primary UV. All of the latter patients had normal serum complement levels (normocomplementemic urticarial vasculitic syndrome; NUVS). No patients with hypocomplementemic UV were encountered. Two patients suffered from necrotizing vasculitis (polyarteritis nodosa, Wegener's granulomatosis); one had a C1-esterase inhibitor deficiency and also demonstrated an immunoglobulin G paraproteinemia. Angioedema occurred in many patients and could not be used as a differential diagnostic feature. The course of the illness was chronic in most patients, lasting for up to 23 years, and the response to therapy was unpredictable, erratic, and unsustained. The use of intravenous "pulse" methylprednisolone, cyclophosphamide, or high-dose oral steroids helped selected patients. Colchicine was dramatically effective in one patient with NUVS of 15 years duration. Azathioprine was not beneficial. None of the five patients with NUVS suffered from severe systemic involvement or renal disease, confirming observations by others that this form of UV represents a milder example of the condition.
Semin Arthritis Rheum 1991 Apr
PMID:Urticarial vasculitis in a connective tissue disease clinic: patterns, presentations, and treatment. 206 75

Synovial tissue from patients with rheumatoid arthritis was enzymatically dissociated, and single cell suspensions were fractionated into subpopulations by centrifugation on continuous Percoll gradients. Five fractions (F1-F5) with densities of 0.991-0.998 gm/ml, 0.998-1.042 gm/ml, 1.042-1.062 gm/ml, 1.062-1.082 gm/ml, and 1.082-1.180 gm/ml, respectively, were prepared. F3 consistently contained the highest number of macrophages, while F2 and F4 contained substantially fewer macrophages. Macrophages present in F2, F3, and F4 were enriched by differential adherence to fibronectin-coated collagen gels. These macrophage-enriched cell preparations were found to be Fc and C3 positive, esterase positive, and peroxidase negative, to stain positively with anti-HLA-DR, anti-Leu-M3, OKM1, and OKM5 monoclonal antibodies, and to show characteristic features of macrophages by electron microscopy. Macrophages from F3 consistently induced neovascularization in rat corneas, while equal numbers of macrophages from F2 and F4 did not. Fibroblastic synovial cells and cells that did not adhere to fibronectin-coated collagen gels did not induce neovascularization. Within the rheumatoid synovium, there appears to be a major subpopulation of macrophages capable of inducing neovascularization, a process vital to the development of the rheumatoid synovial pannus.
Arthritis Rheum 1986 Apr
PMID:Stimulation of neovascularization by human rheumatoid synovial tissue macrophages. 242 91

Fifty dairy goats, of various ages, sexes and breeds were selected for examination on the basis of positive serological reactions to caprine arthritis-encephalitis virus (CAEV). Thirty-one had lung lesions including chronic interstitial pneumonia of caudal or cranioventral lobes, bronchopneumonia, verminous pneumonia, pulmonary cryptococcosis or combinations of these. The only infective agent recovered from all the chronic interstitial pneumonia cases examined was CAEV, which was also recovered from lung tissue of 3 goats with arthritis but no lung lesions. The presence of CAEV in lavaged alveolar macrophages from normal lung tissue and from lungs affected with chronic interstitial pneumonia and verminous pneumonia, and the demonstration of a marked increase in nonspecific esterase staining macrophages in areas of chronic interstitial pneumonia, are discussed in relation to the aetiology of the pneumonia.
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PMID:The pathology and aetiology of lung lesions in goats infected with caprine arthritis-encephalitis virus. 340 Nov 45

Peroxidase-anti-peroxidase (PAP) staining and specific antibodies against cathepsin G and elastase from polymorphonuclear leukocytes (PMN) were applied to pannus-free and microscopically intact superficial articular cartilage. Restricted local deposits containing cathepsin G and elastase were found in three of ten patients with seropositive rheumatoid arthritis (RA), in one of three patients with seronegative RA and in one patient with juvenile chronic arthritis (JCA). Similarly, localized deposits of IgG and C3 were found in the patients with seropositive RA and JCA, but not in the patient with seronegative RA. Adjacent sections exhibited esterase activity in and around the PMN. In proteinase-positive areas from patients with seropositive RA the inhibitors alpha 1-proteinase inhibitor (alpha 1-PI) and alpha 2-macroglobulin (alpha 2-MG) were present in two of three and one of three patients, respectively. In JCA only alpha 1-proteinase inhibitor was present, and in seronegative RA no inhibitors were found. No staining of articular cartilage was observed in a patient with psoriatic arthritis. One of three cases with osteoarthritis exhibited patchy superficial staining for IgG only. In articular cartilage covered by pannus, in three patients with seropositive RA, in one with seronegative RA and in the patient with JCA a few regions with variably dense PMN infiltrates were observed. Cathepsin G, elastase and esterase activity were found in and around the PMN. In one of the three patients with seropositive RA the adjacent cartilage-pannus junction exhibited distinct staining for cathepsin G and elastase, but not for IgG/C3 and proteinase inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Degradation in vivo of articular cartilage in rheumatoid arthritis and juvenile chronic arthritis by cathepsin G and elastase from polymorphonuclear leukocytes. 342 18

The histopathology of arthroscopic biopsy material from the knees of 8 patients with monarticular juvenile rheumatoid arthritis (JRA) of recent onset and of 4 control patients was examined using a histochemical method for acid alpha-naphthyl acetate esterase and an avidin-biotin-peroxidase complex method for different cell subtype-specific surface antigens. According to results of our prospective, single-blind study, nonspecific synovitis was observed in those biopsy samples obtained early in the course of disease. The samples were also characterized by cellular changes that are quite distinct from those described in patients with chronic rheumatoid synovitis. JRA must be considered the cause of symptoms if no orthopedic or infectious disease is found at arthroscopy in children with monarticular symptoms of recent onset and if nonspecific synovitis is observed in the histopathologic specimen. This pathologic description, however, does not correspond to that of classic rheumatoid synovitis. In our studies, we found that mononuclear cells displaying diffuse cytoplasmic esterase and surface Ia formed a large proportion of all inflammatory cells in situ. There were comparatively few activated Ia+ T cells and plasma cells. These observations suggest that exudative features and nonspecific cellular inflammation are prominent at onset of JRA. The immune response, in the form of immunocompetent T and B cells, seems to be more extensively involved in chronic JRA and may represent secondary features of the disease.
Arthritis Rheum 1986 Jan
PMID:The value of biopsy in patients with monarticular juvenile rheumatoid arthritis of recent onset. 351 21

The use of unfixed and undecalcified cryostat sections of mouse knee joints is described for the study of enzyme histochemical reactions. Non-inflamed knee joints and knee joints of mice with antigen induced arthritis have been used. Joints were embedded in gelatin and subsequently cut at low speed with a motor-driven cryostat fitted with a tungsten carbide knife at an obtuse angle (10 degrees). The sections were attached to transparent tape to keep the integrity of the tissue intact. The following histochemical reactions were carried out successfully: the tetrazolium salt reaction for dehydrogenase and reductase activity, the post-azo-coupling method for acid phosphatase and cathepsin B activity and the simultaneous azo-coupling method for esterase activity. In all cases the morphology and integrity of the sections were well kept and serial sections were obtained without any difficulty. Nonspecific staining of the tape did not occur. The localization of the final reaction product was meeting criteria for specific and precise histochemical methods with the exception of the metal salt method because of nonspecific staining of undecalcified bone. Cytophotometry of the final reaction product appeared to be reproducible and valid as demonstrated by reaction for glucose-6-phosphate dehydrogenase activity in synoviocytes from knee joints with induced arthritis. End point measurements as well as kinetic measurements of the formazan production were performed and linear relationships were found between the specific formazan formation and section thickness or incubation time, respectively. It is concluded that cryostat sections attached to transparent tape are an excellent tool for the study of the metabolism in tissues adjacent to bone matrix.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enzyme histochemical reactions in unfixed and undecalcified cryostat sections of mouse knee joints with special reference to arthritic lesions. 381 56

State of the kallikrein-kinin system components (activity of kallikrein and total esterase activity of trypsin-like enzymes) was studied in synovial fluid at the acute period of the knee joint closed injury. The kallikrein activity as well as the esterase activity of trypsin-like enzymes correlated completely with clinical manifestations of the reactive arthritis. These enzymes appear to have a definite importance in development of inflammation in the joint.
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PMID:[Kallikrein-kinin system of the synovial fluid in closed injury to the knee joint]. 384 46

Adherent cells from synovial tissue of rheumatoid arthritis patients were fractionated on Percoll density gradients and analyzed to determine phenotypes, effects on allogeneic T lymphocyte proliferation, and production of prostaglandin E2 (PGE2). Cells expressing HLA-DR predominated in all fractions, and esterase-positive cells were enriched in light fractions. Heavy cells were potent stimulators in the mixed lymphocyte reaction and produced little PGE2, whereas light cells suppressed the mixed lymphocyte reaction and produced a large quantity of PGE2. These results suggest that macrophage-like synovial cells that suppress T helper lymphocyte activity are generated secondary to synovial lymphocyte activation in rheumatoid arthritis.
Arthritis Rheum 1985 Aug
PMID:Different populations of rheumatoid adherent cells mediate activation versus suppression of T lymphocyte proliferation. 387 51

We examined fibronectin synthesis, secretion, and deposition in vitro by primary explants of rheumatoid synovium. Primary cultures initiated from tissue with monocytic infiltrates had higher levels of fibronectin synthesis; addition of dexamethasone at concentrations known to stimulate other tissue fibroblasts increased fibronectin synthesis and secretion. Newly synthesized fibronectin recovered from primary rheumatoid culture medium had a higher apparent molecular weight (240-245 kd), on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, compared with fibronectin recovered from passaged normal and rheumatoid cultures (230 kd). Primary rheumatoid explant cultures had a characteristic morphology which correlated with fibronectin deposition. Dense deposits of fibronectin extracellular matrix covered overlapping synoviocytes adjacent to esterase-positive mononuclear cells. Dexamethasone-treated cultures showed little fibronectin deposited as extracellular matrix and did not develop overlapping cellular networks. Characteristic patterns of fibronectin synthesis and deposition in primary rheumatoid cultures appear to result from interaction between fibroblastic and monocytic cells. This culture system may provide a model by which to study interactions between cells and extracellular matrix components that regulate synovial cell function.
Arthritis Rheum 1985 Sep
PMID:Synthesis, secretion, and deposition of fibronectin in cultured human synovium. 403 55


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