Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mobilization of circulating neutrophils toward an inflamed area involves adherence of the cells to the vascular endothelium and subsequent penetration through the endothelial cell layer without causing significant damage. To investigate the nature of a possible protective mechanism, granulocytes were incubated with the extracellular matrix (ECM) produced by cultured endothelial cells and tested for release of enzymes, chemoattractants, and free oxygen radicals. In the absence of exogenously added stimuli, the neutrophils adhered to the ECM but there was no detectable release of lysozyme, chemotactic activity, or production of O2-. In contrast, the cells readily released a heparan sulfate-degrading endoglycosidase (heparanase) to an extent comparable with that released in contact with polystyrene surfaces. Neutrophils treated with the calcium ionophore A23187 or with the peptide FMLP produced O2- to a much lesser degree when incubated in contact with ECM-coated surfaces than did those incubated in contact with uncoated polystyrene culture dishes. The ECM itself was devoid of superoxide dismutase activity. Stimulation with opsonized zymosan was not inhibited by the ECM. Experiments with isolated constituents of the ECM revealed that fibronectin but not collagen type IV or laminin could partially inhibit O2- production by Ca2+ ionophore-stimulated neutrophils. Treatment of the ECM with proteolytic enzymes, but not with heparanase, abolished its inhibitory effect on neutrophil activation. These results indicate that the subendothelial basement membrane has the capacity to inhibit release of potentially noxious agents excluding heparanase, suggesting a preferential involvement of this enzyme in neutrophil diapedesis.
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PMID:Selective inhibition of neutrophil activation by the subendothelial extracellular matrix: possible role in protection of the vessel wall during diapedesis. 216 83

The ultrastructural and immunohistochemical features of a primary tumor of the ileum showing the classic histologic features of an inflammatory fibroid polyp (IFP) of the gastrointestinal tract are presented. Ultrastructurally the proliferating cells showed a combination of fibroblastic and histiocytic features, with abundant rough endoplasmic reticulum and active production of collagen in many of the cells and long, dendritic cytoplasmic projections with large cytoplasmic vacuoles containing remnants of phagocytosed cellular debris in others. Immunohistochemical studies showed strong cytoplasmic positivity in the proliferating cells with vimentin antibodies and scattered positivity with muramidase. Additional findings include the ultrastructural demonstration of oligocilia and occasional primitive intercellular junctions. The findings in this case suggest that IFP may represent a proliferation of primitive submucosal stromal cells exhibiting incomplete fibrohistiocytic differentiation.
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PMID:Inflammatory fibroid polyp of the small intestine: ultrastructural and immunohistochemical observations. 218 50

Platelets, basophils and neutrophils from a patient with the Wiskott-Aldrich syndrome (WAS) were exposed to stimuli that activate specific membrane receptor or directly initiate biochemical events (e.g. the Ca2+ ionophore A23187 and ionomycin or arachidonic acid). Platelets from this patient did not aggregate in response to ADP, collagen, thrombin or adrenaline, which activate specific membrane receptors. Platelet aggregation, however, was normal in response to compound A23187, ionomycin or exogenous arachidonic acid. Histamine release from basophils of the WAS patient was normal in response to anti-IgE, a formylated peptide (f-met peptide), and to A23187. Similarly, the release of the lysosomal enzymes, beta-glucuronidase and lysozyme, from neutrophils of the WAS patient in response to serum treated zymosan (Zx), f-met peptide, and A23187 was not significantly different from that of his parents and 13 normal donors. These results suggest that the primary defect in WAS is selectively present in platelets and is located in a biochemical step between receptor activation and Ca2+ influx and/or initiation of arachidonate metabolism.
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PMID:The Wiskott-Aldrich syndrome: studies of platelets, basophils and polymorphonuclear leucocytes. 242 57

We investigated the effect of the extracellular protease of Serratia marcescens on human serum constituents such as immunoglobulins, fibronectin, alpha 1-protease inhibitor, alpha 2-macroglobulin, lysozyme, and transferrin. At a very low concentration of Serratia 56-kilodalton protease (56K protease), purified human plasma fibronectin was degraded rapidly into three structural domains or small fragments. Immunoglobulin G3 (IgG3) and IgA1 were also degraded within 30 min with 1 microgram of this protease per ml, more rapidly than their other subclass of IgG or IgA. alpha 1-Protease inhibitor, which did not inhibit the 56K protease, was degraded similarly by the protease. These events were demonstrated by fluorescence polarization and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The protease was considerably inhibited by human alpha 2-macroglobulin and chicken ovomacroglobulin. However, when there was a 2 M excess of ovomacroglobulin or a 4 M excess of alpha 2-macroglobulin over the 56K protease, about 25 or 40% proteolytic activity remained, respectively. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that the protease degraded the alpha 2-macroglobulin extensively during prolonged incubation, which paralleled with regeneration of the protease activity. The protease also cleaved human lysozyme, although moderately. Human serum transferrin was degraded slightly, and human serum albumin was almost resistant to the 56K protease. The enzyme seemed to have no effect on reconstituted collagen, but it degraded rat tropocollagen and yielded fragments of beta and gamma chains by cleaving the intramolecular cross-links. Most of the above proteolysis by the 56K protease appears to result in a limited type of substrate specificity. Thus, the present study demonstrates that the protease is capable of degrading defense-oriented humoral proteins and tissue constituents. Furthermore, it is toxic to fibroblasts. These findings also clarified the possible role of Serratia protease as a virulence factor in the pathogenesis of serratial infections. We recently demonstrated this notion in vivo with rabbit cornea (R. Kamata et al., Ophthalmology 92:1452-1459, 1985).
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PMID:Degradation of protease inhibitors, immunoglobulins, and other serum proteins by Serratia protease and its toxicity to fibroblast in culture. 242 50

In 1059 patients who had transurethral resections (TUR) of the prostate 8 cases (0.8%) with nonspecific granulomas were found. In another group of 280 patients treated by TUR for tumours of the urinary bladder 5 cases (1.8%) had granulomatous lesions in the resectates. The granulomas were observed only in patients with prior surgical trauma of the prostate and the bladder with an incidence of 14% and 6.5%, respectively. None of the patients had systemic diseases. Morphologically, two types of granulomas were observed, foreign-body-type and necrotizing. Carbonization rests were frequently noticed in the granulomatous lesions and the configurations and anatomical distribution of the granulomas suggest a common pathogenesis by electrocauterization. Immunohistochemically, histiocytic cells were stained by antibodies against lysozyme. In the prostate, no reaction by antibodies against prostate specific antigen was observed in the granulomas. The findings are compared to previously reported cases of iatrogenic granulomas in the prostate, the urinary bladder and other organs. It is concluded that the granulomas arise as a local reaction to previous surgery, maybe involving hypersensitivity to locally altered collagen.
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PMID:Iatrogenic granulomas of the prostate and the urinary bladder. 244 82

In order to study human bile duct cells in vitro, cystic ducts were obtained during cholecystectomy and treated with collagenase and mechanical abrasion to isolate biliary epithelial cells. The culture medium was supplemented with 50% of a bovine bile duct conditioned medium obtained by incubating minced bovine extrahepatic bile ducts for 24 hr in Dulbecco's modified Eagle's medium. Cells grew in monolayer and showed contact inhibition at confluency. The epithelial origin of primary cultures was verified by their growth pattern, ultrastructure, and indirect immunofluorescence for cytokeratin. The cultures showed specific immunofluorescence for lysozyme, collagen types I, III, and IV, fibronectin, and laminin, but were negative for collagen type V and factor VIII-associated antigen. Thus, these cultures provide an experimental model for the in vitro study of biliary atresia and other bile duct diseases.
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PMID:Characterization of human extrahepatic biliary duct epithelial cells in culture. 245 76

In vivo-activated interleukin 2 responsive T cell clones were generated from peripheral blood (PB) and synovial fluid (SF) of rheumatoid arthritis (RA) patients and from normal control PB. The specificity of these clones was assessed by measuring proliferation induced by the connective tissue elements (CTE) collagen types I and II, native and denatured, proteoglycans, and irrelevant control antigens. The cloned T cells from RA patients but not from normal subjects responded in vitro with proliferation to all CTE but not to control antigens purified protein derivative, ovalbumin, or lysozyme. Proliferation occurred in the presence and absence of accessory cells (AC), but the responses were consistently higher in the presence of AC. Antibodies to HLA-DR abrogated the proliferative response to CTE suggesting that DR expression was necessary for the induction of proliferation. These findings demonstrate the existence of clonable T cells responsive to CTE in PB and SF of RA patients. Expression of reactivity to CTE may contribute to the chronicity of the inflammation in RA.
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PMID:Interleukin 2 responsive T cell clones from rheumatoid and normal subjects: proliferative responses to connective tissue elements. 246 52

Heat capacity, intrinsic viscosity and ellipticity of a number of globular proteins (pancreatic ribonuclease A, staphylococcal nuclease, hen egg-white lysozyme, myoglobin and cytochrome c) and a fibrillar protein (collagen) in various states (native, denatured, with and without disulfide crosslinks or a heme) have been studied experimentally over a broad range of temperatures. It is shown that the partial heat capacity of denatured protein significantly exceeds the heat capacity of native protein, especially in the case of globular proteins, and is close to the value calculated for an extended polypeptide chain from the known heat capacities of individual amino acid residues. The significant residual structure that appears at room temperature in the denatured states of some globular proteins (e.g. myoglobin and lysozyme) at neutral pH results in a slight decrease of the heat capacity, probably due to partial screening of the protein non-polar groups from water. The heat capacity of the unfolded state increases asymptotically, approaching a constant value at about 100 degrees C. The temperature dependence of the heat capacity of the native state, which can be determined over a much shorter range of temperature than that of the denatured state and, correspondingly, is less certain, appears to be linear up to 80 degrees C. Therefore, the denaturational heat capacity increment seems to be temperature-dependent and is likely to decrease to zero at about 140 degrees C.
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PMID:Heat capacity and conformation of proteins in the denatured state. 253 36

Study of temperature dependence of heat capacity in denatured biopolymers (collagen, elastin, lysozyme, DNA) with 10-15% of bound water revealed a characteristic jump at some critical temperature Tc. It is argued that such behavior reflects glass transition in biopolymers.
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PMID:[Jump-like change in the heat capacity of denatured biological macromolecules]. 261 Dec 91

During the process of extravasation, monocytes transiently adhere to capillary endothelium and subsequently with a variety of extracellular matrix components. These early interactions are likely to serve as modifiers of transcriptional activity and serve to prime monocytes for rapid synthesis of mediators. We have previously reported that adherence to plastic rapidly induced or down-regulated steady-state mRNA levels of a number of monocyte inflammatory mediator genes. We now report that adherence to surfaces pretreated with fibronectin resulted in TNF-alpha and CSF-1 mRNA levels approximating adherence to plastic, whereas adherence to fibronectin, fibronectin/anti-fibronectin complexes, or collagen resulted in markedly decreased levels of CSF-1 induction and lysozyme down-regulation. In contrast, monocyte adherence to collagen induced the highest sustained levels of TNF-alpha expression. PMA, but not the chemotactic factor FMLP, stimulated non-adherent monocytes to express c-fos and TNF-alpha and down-regulate lysozyme mRNA. Although all donors responded to adherence, several failed to produce CSF-1 mRNA after PMA stimulation in the non-adherent state. These data demonstrate that monocyte mediator expression may be more dependent on the selectivity of signals induced by adherence to different substrates than the initial chemotactic response.
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PMID:Human monocyte inflammatory mediator gene expression is selectively regulated by adherence substrates. 278 45


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