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Biomedical subjects

H Pruul

Publications and source records attributed to H Pruul.

26 records · Page 2Linked to original sources
PubMed1982

The effect of exposure of Staphylococcus aureus to penicillin on susceptibility to the bactericidal activity of human leukocytes.

The effect of brief exposure of staphylococci to penicillin upon susceptibility to leukocidal activity was studied. Antibiotic pretreated staphylococci were incubated with normal human leukocytes and viability of the bacteria was determined. Penicillin pretreated staphylococci were more susceptible to killing by leukocytes than untreated control bacteria. The extent of sensitization varied between different strains of staphylococci. When staphylococci were exposed simultaneously to leukocytes and penicillin, the bacteria were protected from the lethal action of penicillin. This study demonstrates that phagocytosed staphylococci are protected from penicillin, but prior exposure to the antibiotic increases their susceptibility to the activity of leukocytes.

Adult↗
PubMed1981

Enhanced susceptibility of Escherichia coli to intracellular killing by human polymorphonuclear leukocytes after in vitro incubation with chloramphenicol.

The effect of brief exposure to chloramphenicol of a pathogenic strain of Escherichia coli on susceptibility to normal human leukocytes was examined. Leukocytes killed chloramphenicol-pretreated E. coli more efficiently than they did untreated controls. Phagocytosis of pretreated bacteria, as measured by the uptake of radiolabeled bacteria and by direct visual count of engulfed bacteria, was not significantly increased. The decrease in viability was associated with enhanced intracellular killing of phagocytosed antibiotic-damaged bacteria. Chloramphenicol pretreatment altered the frequency distribution of intracellular bacteria by decreasing the number of leukocytes containing multiple stainable bacteria. Leukocytes failed to kill chloramphenicol-pretreated E. coli in the presence of phenylbutazone, which allowed an accumulation of intracellular bacteria. These results indicate that exposure of E. coli to chloramphenicol renders the bacteria more susceptible to intracellular killing and degradation.

Blood Bactericidal Activity↗
PubMed1979

Enhancement of leukocyte activity against Escherichia coli after brief exposure to chloramphenicol.

The effect of brief exposure of Escherichia coli to chloramphenicol on the antibacterial activity of normal human leukocytes was studied by following changes in viability of the bacteria in the presence of leukocytes and serum. Growth was suppressed, and the extent of suppression was directly related to the period of exposure and the concentration of chloramphenicol. When exposed to clinically achievable levels of the drug for 10 min, E. coli failed to resume normal growth for 1 to 4 h in the presence of leukocytes and serum after removal of the drug. The post-antibiotic leukocyte enhancement effect required the presence of antibody and complement. This effect demonstrates the importance of early events in the encounter between antibiotic and microorganism in determining the subsequent activity of host defense components.

Blood Bactericidal Activity↗
PubMed1972

Interaction of complement and polymyxin with gram-negative bacteria.

The interaction of complement and polymyxin with gram-negative bacteria has been investigated by using three strains of Salmonella typhimurium in an attempt to determine the loci of complement action. It has been shown that the bactericidal activities of complement and polymyxin towards a smooth gram-negative organism are similarly affected by various components of the bactericidal test system. Further, complement and polymyxin have been shown to act synergistically in the bactericidal event. Evidence is presented which suggests that each agent produces lesions in the outer membrane of gram-negative bacteria, allowing lysozyme to interact with its glycopeptide substrate. An attack on the inner cytoplasmic membrane follows, since cell respiration is rapidly inhibited and this membrane becomes sufficiently disorganized to permit massive leakage of beta-galactosidase from the cytoplasm of the target cells.

Bacteria↗
PubMed1971

Sensitization of complement-resistant smooth gram-negative bacterial strains.

Many gram-negative bacteria are susceptible to the bactericidal action of complement in the presence of specific antibody. As a general rule, rough strains are readily killed, whereas smooth strains are relatively resistant. The results of this study show that the serum sensitivity of smooth gram-negative organisms can be controlled by the environmental conditions imposed by the test system. Smooth organisms which are completely resistant to the bactericidal action of immune serum plus complement in the presence of divalent cations become quite sensitive in a test system containing a relatively high concentration of certain univalent cations; this effect is potentiated by ethylenediaminetetraacetic acid. Since it is generally accepted that the serum resistance of smooth gram-negative organisms is associated with the protection afforded by their thick lipopolysaccharide layer, it is suggested that environmental conditions favoring serum sensitization cause some structural disorganization of the smooth lipopolysaccharide of these cells.

Journal Article↗
PubMed1971

Protective role of smooth lipopolysaccharide in the serum bactericidal reaction.

The mechanism by which smooth lipopolysaccharide (LPS) protects Salmonella typhimurium C5 from the lethal action of specific antibody and complement has been investigated. Tris(hydroxymethyl)aminomethane (Tris) and ethylenediaminetetraacetate (EDTA), which sensitize S. typhimurium C5 to the bactericidal action of immune serum, were shown to cause appreciable structural modification of the smooth LPS associated with these cells. Mg(2+) was shown to reverse the sensitization of C5 by Tris, but this divalent cation was unable to reverse the sensitizing effect of Tris plus EDTA, which, unlike Tris, caused relatively large amounts of O-antigenic components to be released from the C5 cell wall. The possibility that smooth LPS blocks the interaction of activated complement components with receptors on the cell wall is discussed.

Animals↗
PubMedDate not supplied

Postantibiotic leukocyte enhancement: increased susceptibility of bacteria pretreated with antibiotics to activity of leukocytes.

Exposure of Escherichia coli and Staphylococcus aureus to high levels of certain antibiotics for brief periods of time increases the susceptibility of the organisms to the antimicrobial action of normal human leukocytes. The degree of sensitization varies with the antibiotic used for the pretreatment of the bacteria and is most pronounced in pretreatment of E. coli with chloramphenicol. Studies on the rates of phagocytosis and intracellular killing of E. coli indicate that the postantibiotic leukocyte enhancement effect operates through increased susceptibility of antibiotic-damaged bacteria to the intracellular killing mechanisms of leukocytes. These observations may explain the efficacy of antimicrobial dosage regimens in which drug levels are below inhibitory concentrations for part of the dosage interval.

Adult↗