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)

Lysozyme is a dominant member of the antibacterial complex of human saliva and has the potential to kill bacteria by direct lysis or by mechanisms (not completely understood) that are independent of its muramidase activity. The muramidase-independent bactericidal activity appears to depend upon its cationic character. Bacterial death may be due to inhibition of nutrient transport (eg. glucose) and disruption of membrane integrity. This review also describes common bactericidal mechanisms of several cationic peptides/proteins to support the cationic-dependent bactericidal model of lysozyme.
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PMID:Antibacterial mechanisms of lysozyme on Streptococcus mutans. 213 96

Using the monoclonal antibody HAM-56 with the avidin-biotin method on recent or archival paraffin-embedded tissue from multiple sclerosis brains, we have been able to distinguish between acute, chronic active and inactive lesions. HAM-56 stains all macrophages, monocytes and at least some microglia; it is the only pan-macrophage marker to our knowledge that can be satisfactorily used on conventional paraffin sections. A much narrower range of mainly perivascular macrophages in acute plaques of multiple sclerosis is stained with MAC-387, anti-muramidase and anti-alpha1-anti-trypsin. The acute plaques show HAM-56-stained macrophages throughout the lesion, and these macrophages exhibit profiles of phospholipid-rich myelinic bodies, which are also usually stainable with Luxol fast blue. Active ongoing lesions show a rim of macrophages at the edge of the lesion. These macrophages show profiles of large vacuoles, thought to represent the sudanophilic esterified cholesterol formed during demyelination. Inactive cases show none of these features; the few perivascular macrophages present often contain the end product of lipid peroxidation, ceroidlipofuscin.
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PMID:Macrophage histology in paraffin-embedded multiple sclerosis plaques is demonstrated by the monoclonal pan-macrophage marker HAM-56: correlation with chronicity of the lesion. 214 83

Hepatocellular carcinoma with osteoclast-like giant cells (hepatic giant cell carcinoma [HGCC]) is a rare entity, with only three cases reported. The tumor is histologically similar to giant cell tumor (GCT) of bone, and the origin of the multinucleated giant cells and mononuclear stromal cells has not been determined. The purpose of this report is to present a case of this rare tumor and compare its ultrastructural and immunohistochemical features with those of a conventional GCT of bone. Histologically, the HGCC consists of sheets of osteoclast-like giant cells with a background of mononuclear cells. The giant cells lack the pleomorphism seen in hepatocellular carcinomas with anaplastic giant cells. At the light microscopic level, most of this tumor was nearly identical to a GCT of bone, but several microscopic fields (less than 5% of the tumor) had the histologic appearance of a "usual" hepatocellular carcinoma. The hepatic tumor was negative for HAM 56, epithelial cytokeratins, muramidase, and alpha-1-antitrypsin, with only focal positivity for chymotrypsin in mononuclear and giant cells. The GCT was strongly positive for alpha-1-antitrypsin and chymotrypsin in both the mononuclear and giant cells and showed focal, weak staining for AE1 and AE3 in the mononuclear stromal cells. Ultrastructurally, both mononuclear and giant cells of the HGCC showed features typical of hepatocellular carcinoma. Although the patient presented in this report died, the pattern of growth was different from most hepatocellular carcinomas. The overall histologic features of this tumor are distinctive and appear to justify separating this variant from other types of hepatocellular carcinoma.
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PMID:Hepatic giant cell carcinoma. An ultrastructural and immunohistochemical study. 215 1

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

The amino acid composition of cell walls and surface proteins, isolated from virulent (M+) and avirulent (M-) streptococcal strains (group A, type 29) has been determined by the method of E. H. Beachey et al. The kinetics of the lysis and proteolysis of streptococcal cell walls with muramidase and protease obtained from Actinomyces levoris and streptolysin has been studied. The constants describing the progress rates of these processes has been determined; their values in case of both lysis and proteolysis are higher in virulent strains than in avirulent ones.
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PMID:[The physicochemical and biochemical characteristics of the cell walls in M+ and M- variants of Streptococcus group A type 29]. 220 Nov 47

The attachment of capsular polysaccharide to Streptococcus pneumoniae was examined using monoclonal and polyclonal antibodies. Among the strains examined, the capsular polysaccharide of types 2, 4, 6A, 6B, 7F, 8, 14, 19F and 23F was bound to the pneumococci whereas that of a type 3 strain was not. Sequential treatment with 2% SDS at 100 degrees C, pronase, and EDTA did not dissociate the capsular polysaccharide from the pneumococci. Treatment of the cells with mutanolysin, a muramidase that degrades the cell wall peptidoglycan of pneumococci and other streptococci, released both the capsular and the cell wall C-polysaccharide (C-Ps). Type 6A capsular polysaccharide released from cell walls by mutanolysin treatment, was fractionated by high performance liquid chromatography and examined by immunoelectrophoresis. It was found to be bound to both the C-Ps and the peptidoglycan. The bond between the capsular polysaccharide and the peptidoglycan has not yet been identified but is probably covalent, as the two components could not be dissociated after boiling in SDS. Based on our studies with type 6A, we propose that capsular polysaccharide and C-Ps of the pneumococcus are linked to the peptidoglycan at different sites and, thereby, indirectly to each other. Studies in mice showed that the peptidoglycan enhanced the serum antibody response to C-Ps but not to type 6A polysaccharide.
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PMID:Covalent linkage between the capsular polysaccharide and the cell wall peptidoglycan of Streptococcus pneumoniae revealed by immunochemical methods. 221 83

The lysA gene specifying an endolysin of Lactobacillus delbrueckii subsp. bulgaricus bacteriophage mv1, was cloned and expressed in Escherichia coli. The 4.05-kb restriction fragment containing this gene was analysed by restriction and deletion mapping, and by subcloning. The nucleotide sequence of a 1150-bp fragment coding for an active lysin was determined. The lysA gene consists of 585 bp and codes for a protein of a deduced Mr of 21,120, which agrees with the size based on in vivo transcription/translation studies. The deduced amino acid sequence of the mv1 lysin (LysA) was compared to that of other known lytic enzymes. Significant homology was observed with the N-terminal portion of the muramidase of the fungus Chalaropsis and that of the muramidase of the Streptococcus pneumoniae phage Cp-1, suggesting that LysA might be a muramidase. In E. coli, the cloned lysA gene was able to complement the muramidase-defective bacteriophage lambda Ram5, proving that the products of these two genes are interchangeable. The lysA gene is preceded by an open reading frame with unknown function and no characteristic prokaryotic promoter sequences could be detected upstream from lysA, suggesting that this gene is part of an operon.
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PMID:Cloning, expression and sequence analysis of an endolysin-encoding gene of Lactobacillus bulgaricus bacteriophage mv1. 222 53

The mechanism by which the murein sacculus of Escherichia coli is being enlarged during growth was investigated by pulse and pulse-chase labeling with [3H]diaminopimelic acid. Changes in the composition of the sacculus during aging were analyzed in detail by high performance liquid chromatography separation of the muropeptide subunits released after complete muramidase digestion. After pulses as short as 10 s, a group of novel phosphorylated muropeptides was detected. The kinetics of their appearance is consistent with these structures being derived from the undecaprenylphosphate-linked growing points of murein. A complex maturation process of murein took place including a rapid decay of pentapeptide side chains and a 10-fold increase in tripeptidyl moieties. In addition, the total degree of cross-linkage increased from 16 to 25%, partly due to a 3-fold increase in the formation of LD-A2pm-A2pm cross-links. In pulse-chase experiments the cross-linkage started to decrease after a maximum at about 35 min of chase. The kinetics in the distribution of the radioactivity among acceptor and donor part in the major cross-bridges Tetra-Tetra and Tetra-Tri differed from each other substantially, indicating that the latter structure is completely cleaved within three generations, whereas only 40% of Tetra-Tetra is cleaved during the same time. Furthermore, the attachment of the lipoprotein to murein was delayed by about one generation. It is proposed that these findings reflect an inside-to-outside growth mechanism of the murein sacculus of E. coli.
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PMID:Growth pattern of the murein sacculus of Escherichia coli. 222 56

High activity of proinflammatory, type II phospholipase A2 (PLA2) was found in synovial fluids (SF) in inflammatory arthritis. In search for the sources of this PLA2, we cultured human articular chondrocytes and cartilage explants from healthy, osteoarthritic and rheumatoid joints. All cultures, unstimulated by cytokines, released PLA2 extracellularly. Cultures obtained from the deep layers of the cartilage released more PLA2 than those obtained from the superficial layers. Deep layer explants released 0.38 to 18.16 pmol/min/mg protein PLA2/day, whereas superficial layer explants released 0.39-3.18 pmol/min/mg/day. Chondrocyte cell cultures continuously released PLA2, in the first day 909-46347 pmol/min/(10)6 cells and after 9-26 days of culture 166-2115 pmol/min/10(6) cells. PLA2 released from chondrocytes was calcium dependent and had optimum activity at pH 7.5. Cycloheximide markedly inhibited its release. Chondrocyte cultures also released muramidase (LZM) but there was no correlation between PLA2 and LZM release. It may be concluded that cytokine unstimulated human articular chondrocytes synthesize and release PLA2 extracellularly which is similar to that found in the SF. Thus, chondrocytes may possibly serve as one of the sources of intraarticular PLA2.
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PMID:Synthesis and release of phospholipase A2 by unstimulated human articular chondrocytes. 225 99

1. The sequence of renal cellular membrane damage induced by gentamicin was studied in the rat by using the release of alkaline phosphatase, acid phosphatase, muramidase and protein from renal cells as indices of renal damage. 2. The protective effect of a combination of vitamin E and selenium against renal damage was also investigated. 3. Gentamicin (60 mg kg-1 body weight) was nephrotoxic within 12 h of the first dose. 4. The plasma membrane of the renal tubules is damaged before the lysosomal membrane is affected. 5. A combination of vitamin E (1 mg g-1 body weight) and selenium (4 x 10(-3) mg g-1 body weight) attenuates the renal damage induced by gentamicin. Results suggest synergism between vitamin E and selenium in attenuating the renal damage. The possible mechanism of attenuation is discussed. 6. Vitamin E and selenium may have anti-diuretic potential.
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PMID:Vitamin E and selenium in gentamicin nephrotoxicity. 226 Dec 41


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