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)

Gram-negative bacterial pneumonias have been increasingly important as nosocomial infections. The following model was developed to study the pathogenesis and evaluate therapy of such infections. Intranasal instillation of rats with a suspension of 5 x 10(6) Klebsiella pneumoniae caused bronchopneumonia with 24 h. Bacteria were isolated from the lungs in large numbers (greater than 10(5) colony-forming units [CFU] for at least 13 days after inoculation. Thereafter, the viable concentration decreased to about 10(3) CFU at 21 days but increased to 10(4) CFU at 25 days. Mortality rarely exceeded 25%. Plasma zinc concentration decreased, and plasma seromucoid, lysozyme, and alpha2-macrofetoprotein increased during respiratory K. pneumoniae infection in rats. There seemed to be a linear relationship between seromucoid concentration and the concentration of K. pneumoniae in the lung expressed in log10 units. Plasma zinc, alpha2-macrofetoprtoein, or lysozyme levels, however, did not change until the concentration of bacteria retrieved fron lungs exceeded 4 to 5 logs, Analysis of blood samples obtained serially from the orbital sinuses revealed that rats that succumbed to infection had significantly higher levels of seromucoid, alpha2-macrofetoprotein, and lysozyme and lower levels of plasma zinc than infected rats that survived. Progressive increases in seromucoid and particularly in lysozyme and alpha2-macrofetoprotein appeared to be predicative of death. It is postulated that the threshold effect observed for alpha2-macrofetoprotein and lysozyme reflect significant damage to lung tissue, and thus these two variables are good indexes of the severity of this infection. We propose that this model may be of value in elucidating the pathogenesis of respiratory K. pneumoniae as well as in assessing various models of therapy.
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PMID:Pathogenesis of respiratory Klebsiella pneumoniae infection in rats: bacteriological and histological findings and metabolic alterations. 6 1

Squirrel monkeys were inoculated by the intratracheal inoculation of 700 Klebsiella pneumoniae organisms and developed lobar pneumonia in about 24 h. Characteristic clinical findings were fever, anorexia, and coughing. Laboratory findings included leukocytosis or leukopenia (with the latter more prominent in ultimately fatal infections), bacteremia, and shedding of bacteria into the pharynx. Infected monkeys showed increased plasma lysozyme activity as well as increased plasma ceruloplasmin, haptoglobin and alpha1-antitrypsin. The mortality rate was 60%, and the mean time of death was 50.5 h. Pathologically, the disease spread by means of Kohn's pores and other pathways that generally did not involve airways as a means of dissemination until about 30 h. Squirrel monkeys seem to be better models for human respiratory K. pneumoniae infection than rats or mice.
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PMID:Nonhuman primate model for the study of respiratory Klebsiella pneumoniae infection. 10 26

When genetically serum-resistant Escherichia coli, Klebsiella pneumoniae, and Citrobacter freundii, but not Pseudomonas aeruginosa or Proteus mirabilis, were exposed to polymyxin B, they became susceptible to the bactericidal action of normal human and rabbit sera. In constrast, beta-lactam and aminoglycoside antibiotics did not render any serum-resistant bacteria serum-sensitive. Synergy between polymyxin B and the serum bactericidal system could be demonstrated by the addition of polymyxin B to bacteria in vitro, as well as to bacilli in serum from rabbits injected with the antibiotic. Polymyxin B-treated bacteria were killed by normal, lysozyme-depleted, C2-deficient, and hypogammaglobulinemic sera, but not by heated or C6-deficient sera. These findings indicate that polymyxin B-treated bacteria can be killed via the alternative complement pathway. However, C3 and C3b were detected on the surface of serum-resistant E. coli, regardless of whether the bacteria had been treated with polymyxin B. This observation suggests that a change in susceptibility to the alternative complement pathway was not the only explanation for the acquired serum sensitivity. Polymyxin B may also affect a step in the complement sequence beyond the activation of C3, a step that is apparently blocked in serum-resistant gram-negative bacteria.
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PMID:Lethal effect of complement and lysozyme on polymyxin-treated, serum-resistant gram-negative bacilli. 22 75

The in-vitro effect of EDTA-Tris-lysozyme solution on 16 pathogenic bacteria of medical or veterinary importance was determined. Marked decreases in bacterial count occurred with Pseudomonas aeruginosa, Escherichia coli, Moraxella osloensis and Campylobacter fetus, and smaller decreses with Salmonella typhimurium, Shigella boydii, Aeromonas hydrophila, proteus mirabilis, Listeria monocytogenes and Erysipelothrix insidiosa. The test solution had no effect on Klebsiella ozaenae, Brucella canis, Cornynebacterium pyogenes, Coryne, renale, Streptococcus equi and staphylococcus aureus.
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PMID:In-vitro effect of edta-tris-lysozyme solutions on selected pathogenic bacteria. 80 41

Klebsiella serotype K7 is found among the capsule types that are most prevalent in respiratory tract isolates. To evaluate the significance of the K7 antigen in bacteria-leucocyte interactions, K7-encapsulated Klebsiella pneumoniae strains and their non-capsulate mutants were investigated. The K7 isolates were compared to K2-capsulate strains and their respective K- derivatives. K7-capsulate bacteria were less hydrophilic, and more readily phagocytosed and killed by human polymorphonuclear leucocytes (PMNL) than K2 strains. Loss of the K7 antigen resulted in increased surface hydrophobicity but did not affect phagocytosis and killing, whereas loss of the K2 capsule caused greater susceptibility to the phagocytic and killing action of PMNL. Both the K7 and K2 antigen stimulated the extracellular release of lysozyme from neutrophils but not of myeloperoxidase, indicating degranulation of only secondary granules. All K- mutants induced the release of both lysozyme and myeloperoxidase. Our results suggest that, in contrast to the K2 antigen, the K7 capsular polysaccharide does not confer antiphagocytic properties on bacteria. However, the K7 antigen is able to impede the extracellular release of primary granule enzymes.
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PMID:Interaction of Klebsiella capsule type 7 with human polymorphonuclear leucocytes. 133 74

Chemical composition of a substance produced by Klebsiella pneumoniae which is accumulated in chemically defined medium was determined. This substance (the protective factor) protects the bacterium from being killed by normal human serum. Protective factor was treated with DNase, lysozyme and an alkaline protease. The two former enzymes did not affect the protective factor. On the other hand, when alkaline protease was used, the protective activity was totally lost. Results showed that the protective factor is a protein.
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PMID:[Characterization of a substance which protects Klebsiella pneumoniae from the bactericidal effect of normal human serum]. 134 14

Pulmonary surfactant has been shown to play an increasingly important role in bacterial clearance at the alveolar surface in the lung. This study describes a bactericidal mechanism in which ovine pulmonary surfactant induces killing of Pasteurella haemolytica by normal serum. To demonstrate killing, six bacterial species were incubated first with pulmonary surfactant for 60 min at 37 degrees C and then with serum for an additional 60 min at 37 degrees C. P. haemolytica type A1 strains 82-25 and L101, a P. haemolytica type 2 strain, Escherichia coli, and Klebsiella pneumoniae were susceptible and Pasteurella multocida, Serratia marcescens, and Pseudomonas aeruginosa were not susceptible to killing by ovine pulmonary surfactant and normal serum. No bacteria incubated with bovine pulmonary surfactant were killed by normal serum. Although the species origin of pulmonary surfactant was selective, the species origin of serum was not. P. haemolytica incubated with ovine pulmonary surfactant was killed by fetal calf serum, gnotobiotic calf serum, pooled normal sheep serum, pooled normal rabbit serum, and pooled guinea pig serum. Ultrastructurally, killed P. haemolytica suspensions contained dead cells and cells distorted with vacuoles between the cytoplasmic membrane and the cytoplasm. The mechanism of killing did not correlate with concentrations of complement or lysozyme or titers of residual antibody in either the pulmonary surfactant or the serum, and killing was reduced by preincubation of surfactant with P. haemolytica lipopolysaccharide. Preliminary characterization of both surfactant and serum implicate a low-molecular-weight proteinaceous component in the surfactant and serum albumin in the serum. This mechanism may help clear certain gram-negative bacteria from the lungs of sheep as a part of the pulmonary innate defense system.
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PMID:Ovine pulmonary surfactant induces killing of Pasteurella haemolytica, Escherichia coli, and Klebsiella pneumoniae by normal serum. 145 51

A simple RNA isolation method was developed to purify bacterial RNAs from a large number of samples simultaneously in an hour. The method is based on boiling the cells in the presence of Triton X-100 and lysozyme, and then preferential RNA precipitation with ammonium acetate. There is no CsCl centrifugation required. For the nitrogen-fixing bacterium Klebsiella pneumoniae, the depression condition can be maintained during the cell-harvesting process. The intact isolated RNAs appeared to be free of protein, with a yield of 100 micrograms RNA from a 4-ml cell culture of 100 Klett units (10(9) cells/ml). Any DNA present was in a form that did not react with a nifH probe following Northern blotting to nitrocellulose (i.e., was not single-stranded).
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PMID:Two-step isolation of bacterial ribonucleic acid without using a chaotropic agent or cesium chloride centrifugation. 169 54

Lysozyme from equine neutrophil granulocytes was isolated in a pure form by fast performance liquid chromatography, i.e. ion-exchange chromatography and reversed-phase chromatography. The lysozyme lysed Micrococcus luteus, Bacillus subtilis and Staphylococcus lentus and was also bactericidal against the Gram-negative bacteria Escherichia coli, Klebsiella pneumoniae, Bordetella bronchiseptica, and Serratia marcescens. Staphylococcus aureus and Staphylococcus epidermidis were not lysed. The lysozyme was only very slightly bactericidal for S. epidermidis and S. aureus. Equine neutrophil lysozyme was found to be bactericidal for Gram-positive as well as for Gram-negative bacteria without further treatment. Equine and chicken egg white lysozymes were found to be immunologically related when examined using specific antisera against each of them. Both lysozymes also had very similar specific enzymatic activities against M. luteus membranes.
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PMID:Purification of equine neutrophil lysozyme and its antibacterial activity against gram-positive and gram-negative bacteria. 180 22

The ability to inactivate lysozyme was found in representatives of three species of the genus Klebsiella bacteria: K. pneumoniae (117 strains), K. rhinoscleromatis (104 strains), K. ozaenae (90 cultures). The test cultures displayed a different antilysozyme activity, inactivating from 2 to 30 micrograms/ml of the enzyme. Taking into account the lysozyme role in the immunity and chitin synthesis processes in the organism of insects, the inactivation of the enzyme by Klebsiella may be considered as one of possible mechanisms of the entomopathogenic action of these bacteria.
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PMID:[The antilysozyme activity of bacteria in the genus Klebsiella]. 219 Nov 98


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