Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholerogen-toxoid served as a complex vaccine preparation composed of the main pathogenicity factors of cholera vibrio--cholerogen (toxoid), endotoxin and a number of exoenzymes. The preparation contains 65 +/- 7.5% of protein, 12 +/- 1.2% of reducing sugars, 7 +/- 1.2% of lipids, and 2 +/- 0.3% of nucleic acids. Analytic disc-electrophoresis in polyacrylamide gel and immune disc-electrophoresis revealed at least seven individual proteins with the serological activity in the preparation. About 70% of these constituted toxoid proper; the content of O-antigen was 22%. In the cholerogen-toxoid there were revealed seven exoenzymes of cholera vibrio; proteinase, lecithinase, lipase, DNA-ase, RNA-ase, hyaluronidase, amylase. Antibodies against proteinase, lecithinase, amylase and RNA-ase of cholera vibrio were found in the serum of rabbits immunized with cholerogen-toxoid.
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PMID:[Immunochemical and biochemical characteristics of a preventive preparation against cholera, cholerogen-toxoid]. 94 1

In experimental animal models the susceptibility of the mammary gland to neoplastic transformation is related to its degree of development and proliferative activity; this observation led us to determine whether the human breast epithelium also exhibits development-related differences, and whether these differences could be detected in an in vitro system. Normal breast tissue obtained from reduction mammoplasties of 9 patients ranging in age from 18 to 56 years were characterized in both whole mount preparations and organoids obtained after collagenase-hyaluronidase digestion by their degree of development based upon the types of lobules present. Lobules were classified into type 1 (Lob 1), composed of approximately 11 alveolar buds, the less developed; lobules type 2 (Lob 2), of moderate development, composed of approximately 47 ductules each, and lobules type 3 (Lob 3), composed of 80 ductules each, represented the highest level of development. Epithelial organoids obtained after digestion were plated in DMEM:F12 medium supplemented with hydrocortisone, cholera toxin, insulin and 5% horse serum with a calcium concentration of 1.05 mM Ca++. Following attachment, the medium was replaced by medium containing 0.040 mM Ca++. The percentage of attachment of organoids to the flask was greater in cells from Lob 1 (89-99%) and Lob 1+2 (79-100%) than in cells from Lob 3, which had a 53-67% attachment. The total yield of cells after 7 weeks in culture was also greater in cells derived from Lob 1 and Lob 1+2 than in cells from Lob 3. The total yield of cells obtained from primary cultures was not related to the number of organoids plated, but to the degree of development of the gland. The DNA-labeling index (DNA-LI) in intact breast tissue correlated with that in primary cultures; it was greater in Lob 1 and Lob 1+2 than in Lob 3. By flow cytometry, the highest percentage of cells in S-phase was seen in cells with the highest DNA-LI. We concluded that the growth characteristics of mammary epithelial cells in vitro in a low Ca++ medium is modulated by the degree of development and differentiation of the gland.
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PMID:Influence of human breast development on the growth properties of primary cultures. 275 52

Previously described morphological changes in human synovial cell cultures due to cholera enterotoxin (CT) were studied in relation to activation of adenylate cyclase. A single pulse of CT at nanomolar concentration or less induced at least two-fold activation of adenylate cyclase, which persisted for 7 days or more. The enzyme hyaluronidase was found to cause a rapid reversal of the morphological effects of CT. There was also a reduction in adenylate cyclase activity but only with hyaluronidase concentrations greater than those required to produce maximum reversal of the CT-induced morphological changes. Removal of hyaluronidase was followed by reappearance of the CT-associated morphological effects and a slower reactivation of adenylate cyclase. The mechanism by which hyaluronidase produces the observed changes in synovial cells is not known, but might be related to the dispersal of hyaluronic acid gels bound to the surface of these cells.
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PMID:Activation of human synovial cells by cholera enterotoxin: correlation of morphological responses with adenylate cyclase activities, and the reversing effects of hyaluronidase. 621 57

The binding of cholera and tetanus toxins to receptors on the surfaces of teased nerve fibers was used to localize GM1 and G1b-series gangliosides, respectively, by immunocytochemical methods. Native fibers and fibers treated with various hydrolytic enzymes to degrade specific surface components were studied. With native fibers, both toxins bound abundantly to nodes of Ranvier and poorly to the most external, internodal Schwann cell surfaces. Treatment of the fibers with proteases, hyaluronidase, and chondroitin ABC lyase neither eliminated receptors at the nodes nor unmasked receptors over the internodes. The axolemma underlying the paranodal or internodal myelin, exposed by extensive treatment with protease, bound both toxins in large amounts. Neuraminidase action induced cholera toxin receptors on the Schwann cell surface; these receptors were insensitive to protease. The results indicate that GM1 and G1b-series gangliosides are predominantly localized to axonal and glial structures of the node of Ranvier and to paranodal/internodal Axolemma, and that polysialogangliosides not of the G1b-series are present on the internodal Schwann cell surface.
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PMID:Differential expression of gangliosides on the surfaces of myelinated nerve fibers. 650 52

The participation of resident, elicited, and activated macrophage surface components during internalization of tachyzoites of Toxoplasma gondii was analyzed using neuraminidase, phospholipase C, trypsin, protease, and hyaluronidase. Treatment of these macrophages with neuraminidase from Vibrio cholerae, phospholipase C from Bacillus cereus and Clostridium perfringens, protease, and hyaluronidase prior to their interaction with parasites increased the penetration of host cells by T. gondii. Incubation of macrophages with trypsin significantly inhibited the uptake of parasites. Our findings confirm previous observations that treatment of the macrophages with cytochalasin D under conditions that completely block the typical phagocytic process partially inhibits infection of the cells by T. gondii. The results of simultaneous treatment of the macrophages with enzymes and cytochalasin D suggested that the observed enhancement of cell infection by treatment with neuraminidase and hyaluronidase was attributable to a classic phagocytic process, whereas that obtained using phospholipase resulted from active penetration.
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PMID:Effect of various digestive enzymes on the interaction of Toxoplasma gondii with macrophages. 847 28

Serogroup A strains of Pasteurella multocida, the major cause of fowl cholera, are resistant to phagocytosis in nonimmunized birds. Adherence studies with a capsulated strain of P. multocida (serotype A:3) and turkey air sac macrophages in culture showed that the bacteria were capable of adhering in large numbers to the macrophages but were not internalized. A noncapsulated variant of the bacteria (serotype -:3) showed little or no adherence and was not internalized. These data indicated that the adhesive properties were caused by the presence of a capsule on the bacteria. The role of capsular hyaluronic acid in adherence to macrophages was investigated. Depolymerization of the bacterial capsule with hyaluronidase increased phagocytosis by macrophage cultures, and addition of hyaluronic acid to the macrophages inhibited bacterial adherence. Additionally, exposure of macrophages to chondroitin sulfate B, an anionic polysaccharide similar to hyaluronic acid, did not affect the adhesive properties and resistance to phagocytosis of capsulated organisms. Treatment of macrophages with sodium metaperiodate or trypsin suppressed bacterial binding. Collectively, these data indicate that P. multocida adhesion to air sac macrophages, but not internalization, is mediated by capsular hyaluronic acid and suggest that recognition of this bacterial polysaccharide is a result of a specific glycoprotein receptor.
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PMID:Capsular hyaluronic acid-mediated adhesion of Pasteurella multocida to turkey air sac macrophages. 898 Aug 21

The ability of bacteria to survive in serum is considered a likely virulence determinant in diseases where the infective bacteria become septicaemic. Optimal conditions were established to test the survival of Pasteurella multocida in chicken serum. Serum was used at 90%, the inoculum was 10(3)-10(4)cfu in phosphate buffered saline pH 7.4. Survival was measured after incubation for 2-4 h; if survival was <50% the strain was considered serum susceptible. Susceptible strains were either killed or their growth was inhibited. Some resistant strains not only survived but grew rapidly in unheated serum. Thirty-five strains, all originally isolated from clinical fowl cholera, were tested; eight were susceptible, of which three were killed and five inhibited, and the remainder (27) were resistant. Ten serum-resistant P. multocida serogroup A strains were grown in hyaluronidase to remove the capsule and survival in chicken serum was re-tested. Three strains became susceptible, while seven strains remained resistant. Three serum susceptible strains were then tested in the presence of cytidine monophosphate-N-acetylneuraminic acid (CMP-NANA). This substance is present in the human serum, and is known to mask the effect of complement on Neisseria gonorrhoeae rendering susceptible strains resistant. Two of the three serum susceptible strains became resistant in the presence of CMP-NANA. Serum susceptibility/resistance was more complex than that of Escherichia coli, and the role of resistance to avian complement in the pathogenesis of fowl cholera remains to be determined.
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PMID:Survival of avian strains of Pasteurella multocida in chicken serum. 1069 11

Growth in serum of Pasteurella multocida and related species in chicken, turkey, duck and pig sera were compared, and selected serum-resistant and serum-sensitive strains were inoculated into 18-week-old layers. Eighty-seven field strains of Pasteurella spp. and nine reference strains representing different clones defined by restriction endonuclease analysis (REA) profiles were used in the study. Serum activity was measured by changes in the optical density (OD) of the serum after inoculation and incubation at 41 degrees C for chicken, turkey and duck serum and 39 degrees C for pig serum. Serum activity was measured by comparison with previously determined serum-resistant (P-1059) and serum-sensitive (CU vaccine) strains, and classified into highly serum-resistant, moderately serum-resistant and serum-sensitive. Strains of the same REA type were found to have identical growth curves and the same maximum OD values when tested in serum from the same host species. Turkey serum was shown to be less inhibitory to a wide range of P. multocida strains than chicken, duck and pig sera. Serum-resistant strains were demonstrated among avian as well as mammalian strains. Among the avian strains, the proportion of serum-resistant strains was higher in outbreak strains than in strains from apparently healthy carriers. Removal of the capsule from selected strains by hyaluronidase treatment failed to change the serum activity. The most severe lesions in experimentally infected chickens were produced by a serum-resistant strain; however, lesions were also found in chickens infected by serum-sensitive strains, indicating the involvement of multiple factors in the virulence of P. multocida. Further investigations on serum resistance are indicated in order to relate other host and bacterial factors responsible for the development of fowl cholera.
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PMID:Serum resistance of Pasteurella multocida in avian and porcine sera, and comparative virulence investigations of selected serum-sensitive and resistant strains in chickens. 1239 64