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)

Many clinical abnormalities in atopic eczema have been attributed to an imbalance in autonomic nervous system control, specifically a partial blockade of beta-adrenergic responsiveness. The lysosomal enzyme beta-glucuronidase is released from granulocytes during in vitro incubation with complement-activated zymosan particles. Isoproterenol will inhibit the release of this lysosomal enzyme from the granulocyte and the isoproterenol effect is associated with increased granulocyte cyclic AMP formation. In atopic eczema and asthma, this granulocyte response to isoproterenol is impaired. Histamine also inhibits in vitro zymosan induced release of beta-glucuronidase and this is an H2 histamine effect. In asthma, this H2 histamine response is diminished. In the following study, we found a similar impairment in histamine inhibition of beta-glucuronidase release and formation of granulocyte cAMP in atopic eczema. This defect was found only in granulocytes from patients with active eczema. Thus in active atopic eczema, defects in the pharmacological response of the granulocyte are not limited to beta-adrenergic agonists but include H2 histamine activity.
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PMID:Impaired H2 histamine granulocyte response in active atopic eczema. 22 50

In vitro degranulation of polymorphonuclear leukocytes, which were stimulated either with synthetic chemotactic peptide (N-formyl-methionyl-leucyl-phenylalanine, FMLP) or with C3b-opsonized zymosan as a promotor of phagocytosis, was studied in 66 patients with psoriasis, 18 lesion-free psoriatics, 18 healthy subjects, and 14 other dermatological disorder controls. Stimulated release of lysozyme (from specific granules and azurophil granules) and beta-glucuronidase (from azurophil granules) in the presence of both FMLP and serum-activated zymosan was markedly reduced in patients with actively spreading guttate psoriatic lesions, in whom relapse of lesions lasted for less than 1 month and papules involved about 13-25% of skin surface. In contrast, stimulated degranulation was within normal range in active plaque psoriasis, stationary plaque psoriasis, symptomless psoriatics, and patients with disseminated eczema. Spontaneous release of lysozyme and beta-glucuronidase (background) was found to be not different in all groups studied; however, patients with active guttate psoriasis had significantly lower total lysozyme activity than those with active and stationary plaque psoriasis as well as psoriatics in the remission. These data are in favor of in vivo activation of neutrophils in active guttate psoriasis by some factors related to the early relapse of the lesions. This results in a possible combination of the following phenomena: (1) in vivo partial degranulation of neutrophils; (2) induction of "unresponsiveness state" of these cells to subsequent in vitro stimulation; and/or (3) migration of highly responsive neutrophils to skin lesions, which leaves in the circulation the subpopulation less reactive to chemotactic and phagocytic stimuli.
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PMID:Decreased extracellular release of granule enzymes from in vitro-stimulated polymorphonuclear leukocytes in guttate psoriasis. 371 May 63