Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chronic Erysipelas-polyarthritis in pigs has been considered an animal model resembling human rheumatoid arthritis. Fifteen specifically pathogenfree (SPF) pigs 45 days old were experimentally infectec with strain T 28 of Erysipelothrix rhusiopathiae-bacteria. During the subsequent 32 weeks several enzymatic, immunohistological and microbiological parameters were monitored. Compared to 5 age and sex matched healthy controls the infected pigs showed increased activity of plasma acid phosphatase starting 4 weeks after the infection. Acid phosphatase activity was usually enhanced in synovial fluid of chronically ill animals. Histochemically increased activity of acid phosphatase, beta-glucuronidase and beta-acetylglucosaminidase was found in lining cells and fibroblasts of the synovial membrane of chronically diseased joints. Immunohistochemically Erysipelas-antigen was demonstrated in the synovial membrane even of those inflamed joints from which no living bacteria had been isolated. The microbiological and immunohistochemical results correlated positively with the enzymehistochemical data. The release of lysosomal enzymes from cells of the synovial membrane in chronically diseased joints due to the influence of Erysipelas-bacteria and the possible implications of persistent bacteria on the perpetuation of chronic Erysipelas-polyarthritis are discussed.
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PMID:[Enzyme, enzyme-histochemical and immunohistological studies in chronic erysipelas polyarthritis of swine]. 63 67

The in vitro functions of highly purified blood monocytes were studied in 11 patients suffering from acute bacterial infections (e.g. erysipelas, appendicitis, abscesses). Chemotaxis, superoxide-anion generation, and beta-glucuronidase release of the patients' monocytes in response to the receptor-dependent stimuli formyl-methionyl-leucyl-phenylalanine (FMLP), complement split product C5a, leukotriene B4 (LTB4), and opsonized zymosan particles were measured. All the patients were examined in a follow-up study during the course of illness. A group of 33 healthy volunteers served as control. The patients revealed a transient decrease in monocyte chemotactic migration in response to all stimuli between days 3 and 5 after onset of clinical symptoms. Superoxide-anion generation from patients' monocytes was found to be enhanced 3 days after impaired chemotaxis. Stimulated release of lysosomal beta-glucuronidase showed a decrease in the first days of the disease. However, spontaneous beta-glucuronidase release was enhanced between days 3 and 7 in the patients' monocytes. Serial measurements of monocyte responsiveness. These results indicate a distinct modulation of monocyte functions during the course of an acute bacterial infection. Changes in monocyte maturity and/or activation under inflammatory conditions may be responsible for these alterations in monocyte function.
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PMID:Modulation of human monocyte functions during acute bacterial infection. 284 55

Chemotactic migration, production of superoxide anion (O2-), and the release of beta-glucuronidase from azurophilic granules were determined in polymorphonuclear leukocytes (PMN) from 135 patients with infectious (e.g., pyoderma, acne conglobata, erysipelas) as well as noninfectious (psoriasis) skin diseases. Purified C5a and the formylated tripeptide FMLP were used as stimuli. In addition, longitudinal profiles of PMN activities were performed at daily intervals in several patients. There was a complete absence of PMN responses (chemotaxis, O2--production, and enzyme release) specifically induced by C5a in 25 patients suffering from various inflammatory diseases of the skin. In these patients PMN responsiveness for the tripeptide FMLP was either normal or increased. The C5a-dependent defect of PMN was transient and correlated with disease activity. When normal PMN were incubated with sera from C5a-defective patients, no inherent stimulatory or inhibitory activities compared to control sera were seen. Pretreatment of normal PMN in vitro with various concentrations of C5a failed to completely deactivate PMN without affecting FMLP dependent functions. These observations demonstrate the presence of a functional defect in circulating PMN during acute cutaneous inflammation. The in vitro experiments suggest transient blocking of C5a-dependent PMN functions by a cell-bound factor which seems not to be C5a or C5adesarg.
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PMID:Transient absence of C5a-specific neutrophil function in inflammatory disorders of the skin. 316 55

Circulating human neutrophils from patients with severe inflammatory disorders such as erysipelas and sepsis are specifically desensitized to complement factor C5a stimulation but not to stimulation with other stimuli like N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-8 (IL-8), leukotriene B4 (LTB4), or platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine). In this study, we raised the question whether factors released from polymorphonuclear leukocytes (PMNs) can specifically down-regulate C5a-dependent neutrophil functions. When neutrophils were preincubated with either neutrophil lysates or neutrophil degranulation supernatants, a complete inhibition of C5a-stimulated beta-glucuronidase release and chemotaxis could be observed, whereas FMLP-, IL-8-, LTB4- or PAF-dependent functions were not affected. Serine protease inhibitors like phenylmethylsulfonyl fluoride, antileukoprotease, or elafin abolished this effect. High-performance liquid chromatography of neutrophil degranulation supernatants revealed pronounced inhibition of C5a-dependent neutrophil functions in fractions exerting elastase or cathepsin G activity, but not in fractions exerting proteinase 3 activity. Using purified human leukocyte elastase (HLE), C5a responses like intracellular calcium influx, beta-glucuronidase release, and chemotaxis were also specifically inhibited. Our experiments show that the release of HLE or cathepsin G from neutrophils specifically down-regulates the responsiveness of neutrophils to C5a. Elastase and cathepsin G may therefore play an important role in the down-regulation of acute inflammation.
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PMID:Human leukocyte elastase and cathepsin G are specific inhibitors of C5a-dependent neutrophil enzyme release and chemotaxis. 1514 22