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)

Pentoxifylline has been used for several years in various types of peripheral and cerebrovascular diseases because of its hemorheological properties: pentoxifylline improves the red cell deformability, decreases platelet and red cell aggregation, decreases fibrinogen and plasma viscosity. Its new properties on the leukocyte function can lead to new therapeutical ways. Adherence and peroxidative free radicals production are induced by inflammatory cytokines (IL1, TNF) and can induce vascular tissue damages and development of atherosclerosis. Pentoxifylline has no effect on the normal leukocyte function. However, in all inflammatory diseases, Pentoxifylline acts on the activated neutrophil function: Pentoxifylline decreases adherence to endothelial cells or other surfaces, the superoxide and lysozyme release, and increases chemotaxis. In some animal models of shock and infection, pentoxifylline decreases cellular and tissue damages, mediated by activated neutrophils. Furthermore, in inhibiting neutrophil adhesion to cultured endothelium cells, pentoxifylline, modulates leukocyte-endothelium and leukocyte-platelets interactions which are important factors in the development of inflammation and thrombosis. Pentoxifylline increases the leukocytes mediated activation of fibrinolytic pathways and could play an important role in the prevention of thrombosis. In addition to its well-known effects on chronic vascular diseases, pentoxifylline is also effective in some acute injuries in animal models. This can lead to new research fields allowing a better understanding of atheromatous processes.
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PMID:[New aspects of the pharmacology of pentoxifylline]. 265 14

It has been suggested that focal glomerulosclerosis (FGS) is analogous to atherosclerosis. Because monocytes and their derivatives are involved in the latter, these cells may be involved in the development of the former. To investigate this possibility a combined histochemical and ultrastructural study of FGS was done. Sections from 13 biopsies showing FGS were stained for either nonspecific esterase or lysozyme to detect monocytes and their derivatives. These include foam cells (lipid-containing macrophages) in which there was positive cytoplasmic staining for both nonspecific esterase and lysozyme. Twenty-one of 29 glomeruli (72%) with segmental sclerotic lesions contained monocytes and/or foam cells, whereas only 18 of 251 glomeruli (7%) without the lesions demonstrated these cells (p less than 0.0001). The mean number of monocytes and/or foam cells in segmentally sclerotic glomeruli was 2.0 +/- 1.7 compared with 0.2 +/- 0.3 for uninvolved glomeruli (p less than 0.01). In glomeruli with sclerotic lesions foam cells predominated over monocytes. Neutral lipid was observed focally and segmentally in 29 of 35 biopsies with FGS. Electron microscopy in 23 biopsies consistently demonstrated intracapillary cells with monocytic features but few foam cells in very early lesions characterized by epithelial cell changes but no or minor glomerular tuft alterations. With progression, the relative number of monocytes declined but foam cells were observed more frequently. These results suggest that monocytes and their derivatives are involved in the development of FGS.
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PMID:Monocytes and focal glomerulosclerosis. 279 89

A total of 13 forty-day-old male Japanese quails had free access to a atherogenic diet containing 15% corn oil and 2% cholesterol or commercial basal diet for 3 months. Birds fed basal diet showed no significant intimal lesions. These birds had two types of cells, i.e. smooth muscle cell and fibroblast-like cell, in the tunica media of the ascending aorta. While fat-fed birds showed marked lipid-rich intimal lesions in the ascending aorta but not in the abdominal aorta. Some macrophage-derived foam cells, which were stained for lysozyme and OKM1, were demonstrated in the superficial portion of the thickened intima. The majority of the cells in the lipid-rich thickened intima showed ultrastructural character of fibroblast-like cells with or without lipid droplets. Alpha-1-antichymotrypsin was positive for fibroblast-like cells in the thickened intima but not for those in the tunica media of the ascending aorta. These results suggest that metaplasia of the medial fibroblast-like cells is responsible for the development of atherosclerosis in the quail.
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PMID:[Immunohistochemical and ultrastructural study of aortic lesions in fat-fed quails]. 326 Aug 71

A series of biochemical and morphological studies has focused on the properties and origins of lipid laden foam cells in experimentally induced atherosclerosis in rabbits. Lipids inclusions present in these cells occupy half or more of the cytoplasmic volume and are of two kinds: cytoplasmic lipid droplets composed predominantly of cholesteryl esters and lysosomes in which substantial quantities of free cholesterol have accumulated. The foam cells exhibit some properties of macrophages but not others. They possess high levels of acid hydrolases and catalase and Fc membrane receptors can be detected on their surface. Only about one third of the foam cells, however, exhibit C3 receptors and few if any of the cells appear to contain or secrete lysozyme.
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PMID:Characterization of foam cells in experimental atherosclerosis. 693 40

We studied the antigenic markers of macrophages (Mphs) in atherosclerotic human arteries by immunohistochemistry and compared them with the patterns in Mph subpopulations of tonsil and lymph node, which are also described. The staining of atheroma intimal Mphs was assessed semiquantitatively in the subendothelial, mid, and outer intima. Three patterns of reactivity with Mph antibodies were recognized. (a) Pan-Mph (antibodies HAM56, EBM11, and CD14 group). Staining was maximal in the mid-intimal zone. (b) Subendothelial Mphs (anti-muramidase, anti-alpha-1-antitrypsin and MAC387). In lymphoid tissue, sinusoidal Mphs and a few inflammatory Mphs were stained, as well as blood monocytes. This group of antibodies recognizes Mphs that are likely to be recently blood-derived (RBD-Mphs). (c) Antibodies reactive with various histiocyte populations in lymphoid tissues (anti-Factor XIII; anti-HLA Class II and LN2) also gave maximal staining in the mid-intimal zone, but differences between lesion types suggest that they are recognizing heterogeneous subpopulations of Mphs. These observations demonstrate the heterogeneity of tissue Mphs and suggest that an insight into the dynamics of tissue Mphs can be obtained from the cell phenotype. They indicate that all stages of atherosclerosis can have an outward traffic of Mphs from the blood through the arterial intima.
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PMID:The immunohistochemical heterogeneity of atheroma macrophages: comparison with lymphoid tissues suggests that recently blood-derived macrophages can be distinguished from longer-resident cells. 750 8

Inflammatory reactions induce the production of reactive oxygen species (ROS): the reverse sequence of these events is also true. Moreover, many components of these reactions interact with a synergistic effect. In this short comprehensive review we analyze some of these interactions which may have pathological effects. Inflammatory reactions are triggered off by exogenous or endogenous aggressions and are characterized by cellular and vascular events. The activated leucocytes leave the circulating blood and reach the site of the aggression where they release a large amount of ROS as well as the content of their granules. The granular content is made in a large part by molecules with killing and degradative activities such as myeloperoxidase, defensins, elastase, collagenase, cathepsins and lysozyme. The inflammatory reaction is beneficial for humans when its effects are limited to the pathogens. The insufficiency of a component of the inflammatory reaction such as the production of ROS which is seen, for example in chronic granulomatous disease, leads to severe and recurrent bacterial infections. In other situations inflammatory reactions are deleterious because they are directed against normal tissues instead or in addition to pathogens. In some cases the behaviour of the phagocytes is modified because they have been primed by inflammatory molecules such tumor necrosis factor, LPS, interleukins or interferons. Priming often leads to a decreased speed of locomotion of the leucocytes with an increased susceptibility to their stimuli. The combination of these effects leads to a premature release by the phagocytes of their killing and degradative factors. Production of ROS such as that seen during irradiation, drug metabolism, or ischemia followed by reperfusion for example, induces inflammatory reactions with a secondary amplification of ROS production. Acute ROS production can also lead to thrombosis, whereas chronic ROS production can induce a chronic inflammatory reaction of the endothelium with atherosclerosis as a possible consequence. Some examples are also given to show that ROS might control positively or negatively the activity of inflammatory molecules. The multiplicity of the cross reactions between ROS and inflammation allows to suggest that drugs that disconnect these two events might be therapeutically used.
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PMID:[Reactive oxygen species and inflammation]. 801 8

It is generally accepted that the foam cells in atherosclerotic lesions are derived mainly from monocytes/macrophages. We investigated whether the macrophage-derived foam cells, isolated from the atherosclerotic lesions of cholesterol-fed rabbits, would exhibit properties similar to those of blood monocytes in vitro and whether the cholesterol concentration of the macrophage-derived foam cells would decrease in the presence of an appropriate cholesterol acceptor in culture. We found that most (> 98%) of the foam cells isolated from atherosclerotic lesions were positive for anti-monocyte-macrophage antibody and nonspecific esterase. While almost all (> 98%) of the foam cells exhibited NaF-resistant, nonspecific esterase activity, the blood monocytes exhibited no such activity. Macrophage-derived foam cells contained larger amounts of cholesterol, most of it esterified, than the blood monocytes. Although blood monocytes exhibited a substantial amount of lysozyme, the freshly isolated, macrophage-derived foam cells showed no detectable lysozyme activity. The production of superoxide by macrophage-derived foam cells stimulated by PMA or opsonized zymosan was lower than that of stimulated monocytes. The cholesterol concentration of macrophage-derived foam cells decreased during five days of culture in the presence of an appropriate acceptor, such as normal and hypercholesterolemic rabbit serum and high density lipoprotein, although the rate of decrease was slow. Results suggest that macrophage-derived foam cells may be involved in both the progression and the regression of early atherosclerotic lesions.
Atherosclerosis 1997 Dec
PMID:Characteristics of macrophage-derived foam cells isolated from atherosclerotic lesions of rabbits. 943 Mar 74

Hypochlorite-oxidized low-density lipoprotein ((-)OCl-LDL) has been shown to stimulate various functions of human polymorphonuclear leukocytes (PMNLs). Incubation of PMNLs with (-)OCl-LDL (produced by incubation of 0.4 mM LDL cholesterol with 1 mM NaOCl for 40 min at 37 degrees C) but not native or copper-oxidized LDL induced a substantial generation of reactive oxygen species (ROS) as measured by means of chemiluminescence with one peak at 10-12 min. Upon stimulation with (-)OCl-LDL about 70% of ROS (hydrogen peroxide and superoxide anion) were released from the cells into the extracellular environment. The (-)OCl-LDL-induced increase of the respiratory burst was dependent upon the dose, exposure time, and extent of LDL oxidation. Cytochalasin B, an inhibitor of phagocytosis, markedly diminished the LDL-induced ROS generation to nearly 40% of control values. (-)OCl-LDL enhanced the adhesion of PMNLs to human umbilical venous endothelial cells 2.5-fold as compared to native LDL and promoted the secretion of the active granule enzymes lysozyme and beta-glucuronidase. Together, the results suggest a potential role of LDL-activated PMNLs in initiating and/or maintaining the inflammatory process during the early phase of atherosclerotic lesion development. Alternatively, PMNLs may also play a protective role by phagocytosing oxidized LDL and, thus, preventing further detrimental atherogenic effects of oxidized LDL.
Atherosclerosis 1998 Feb
PMID:Hypochlorite-modified low-density lipoprotein stimulates human polymorphonuclear leukocytes for enhanced production of reactive oxygen metabolites, enzyme secretion, and adhesion to endothelial cells. 954 3

Class A scavenger receptors (SR-A) have several proposed functions that could impact atherosclerosis and inflammatory processes. To define the function of SR-A in vivo, we created C57BL/6 transgenic mice that expressed bovine SR-A under the control of the restricted macrophage promoter, lysozyme (lyso-bSR-A). bSR-A mRNA was present in cultured peritoneal macrophages of transgenic mice and tissues that contain significant macrophages including spleen, lung, and ileum. Functional overexpression of SR-A was demonstrated in peritoneal macrophages both by augmented cholesterol ester deposition in response to AcLDL and enhanced adhesion in transgenic mice compared with nontransgenic littermates. To determine whether macrophage-specific expression of bSR-A regulated inflammatory responses, granulomas were generated by subcutaneous injection of carrageenan. Granuloma size was significantly increased in lyso-bSR-A transgenic mice compared with wild-type littermates [421 +/- 51 mg (n = 11) vs. 127 +/- 22 mg (n = 10), P < 0.001]. However, the larger granulomas in lyso-bSR-A transgenic mice were only associated with an increase in unesterified cholesterol, and not cholesterol esters. Furthermore, granulomas from transgenic mice had an increase in the number of macrophages within the tissue.Therefore, macrophage expression of bSR-A increased presence of this cell type in granulomas without enhancing the deposition of cholesterol esters, consistent with a role of the adhesive property of the protein.
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PMID:Macrophage-specific expression of class A scavenger receptors enhances granuloma formation in the absence of increased lipid deposition. 1144 Nov 31

Class A scavenger receptors (SR-A) have been implicated in the atherogenic process, although there have been conflicting reports as to their specific effect on the development of lesions. In part, this discord may arise because of the variable contribution of SR-A in the several cell types known to express this protein. To determine the effects of macrophage-specific SR-A expression in the atherogenic process, transgenic mice were created using the chicken lysozyme (lyso) promoter to drive expression of bovine SR-A (bSR-A). To express this gene in an atherosclerosis-susceptible strain, bone marrow cells from transgenic and non-transgenic littermates were used to repopulate lethally-irradiated female LDL receptor (LDLr)(-/-) mice. Following hematopoietic engraftment, mice were placed on a diet enriched in saturated fat and cholesterol. After 8 weeks, there was a modest, but statistically significant reduction in serum total cholesterol in LDLr(-/-) mice repopulated with lyso-bSR-A transgenic cells, due to decreased LDL-cholesterol. The extent of atherosclerosis was reduced in both cross-sectional analysis of the aortic root and en face analysis of the intimal surface of the aortic arch. In addition to changes in atherosclerosis, lyso-bSR-A repopulated LDLr(-/-) mice had a marked increase (3.6x) in spleen weights and a disruption of spleen white pulp formation. Therefore, macrophage-specific overexpression of SR-A resulted in reduced atherosclerosis in two vascular beds, reduced serum cholesterol concentrations, and changed the morphology of the spleen.
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PMID:Macrophage-specific expression of class A scavenger receptors in LDL receptor(-/-) mice decreases atherosclerosis and changes spleen morphology. 1217 64


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