[Behavior of bacteriolysis of bacteriolysis of lysozyme in tears, saliva and nasal secretion of full-term and premature infants].
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Anti-Infective Agents, Local↗
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Studies on the immune bacteriolysis. 13. Leakage of enzymes from Escherichia coli during immune bacteriolysis.
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Alkaline Phosphatase↗
[Studies on the immune bacteriolysis. XIV. Requirement of all nine components of complement for immune bacteriolysis].
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Animals↗
The role of bacteriolysis in the pathophysiology of inflammation, infection and post-infectious sequelae.
The literature dealing with the biochemical basis of bacteriolysis and its role in inflammation, infection and in post-infectious sequelae is reviewed and discussed. Bacteriolysis is an event that may occur when normal microbial multiplication is altered due to an uncontrolled activation of a series of autolytic cell-wall breaking enzymes (muramidases). While a low-level bacteriolysis sometimes occurs physiologically, due to "mistakes" in cell separation, a pronounced cell wall breakdown may occur following bacteriolysis induced either by beta-lactam antibiotics or by a large variety of bacteriolysis-inducing cationic peptides. These include spermine, spermidine, bactericidal peptides defensins, bacterial permeability increasing peptides from neutrophils, cationic proteins from eosinophils, lysozyme, myeloperoxidase, lactoferrin, the highly cationic proteinases elastase and cathepsins, PLA2, and certain synthetic polyamino acids. The cationic agents probably function by deregulating lipoteichoic acid (LTA) in Gram-positive bacteria and phospholipids in Gram-negative bacteria, the presumed regulators of the autolytic enzyme systems (muramidases). When bacteriolysis occurs in vivo, cell-wall- and -membrane-associated lipopolysaccharide (LPS (endotoxin)), lipoteichoic acid (LTA) and peptidoglycan (PPG), are released. These highly phlogistic agents can act on macrophages, either individually or in synergy, to induce the generation and release of reactive oxygen and nitrogen species, cytotoxic cytokines, hydrolases, proteinases, and also to activate the coagulation and complement cascades. All these agents and processes are involved in the pathophysiology of septic shock and multiple organ failure resulting from severe microbial infections. Bacteriolysis induced in in vitro models, either by polycations or by beta-lactams, could be effectively inhibited by sulfated polysaccharides, by D-amino acids as well as by certain anti-bacteriolytic antibiotics. However, within phagocytic cells in inflammatory sites, bacteriolysis tends to be strongly inhibited presumably due to the inactivation by oxidants and proteinases of the bacterial muramidases. This might results in a long persistence of non-biodegradable cell-wall components causing granulomatous inflammation. However, persistence of microbial cell walls in vivo may also boost innate immunity against infections and against tumor-cell proliferation. Therapeutic strategies to cope with the deleterious effects of bacteriolysis in vivo include combinations of autolysin inhibitors with combinations of certain anti-inflammatory agents. These might inhibit the synergistic tissue- and- organ-damaging "cross talks" which lead to septic shock and to additional post-infectious sequelae.
Animals↗
Bactericidal cationic peptides can also function as bacteriolysis-inducing agents mimicking beta-lactam antibiotics?; it is enigmatic why this concept is consistently disregarded.
Although there is a general consensus that highly cationic peptides kill bacteria primarily by injuring their membranes, an additional hypothesis is proposed suggesting that a large variety of cationic peptides might also render bacteria non viable by activating their autolytic wall enzymes - muramidases (a "Trojan Horse" phenomenon), resulting in bacteriolysis. This group of cationic peptides includes: lysozyme, lactoferrin, neutrophil-derived permeability increasing peptides, defensins, elastase, cathepsin G, and secretory phopholipase A2. In this respect, cationic peptides mimic the bactericidal/bacteriolytic effects exerted by of beta-lactam antibiotics. Bacteriolysis results in a massive release of the pro-inflammatory cell-wall components, endotoxin (LPS), lipoteichoic acid (LTA) and peptidoglycan (PPG), which if not effectively controlled, can trigger the coagulation and complement cascades, the release from phagocytes of inflammatory cytokines, reactive oxygen and nitrogen species, and proteinases. Synergism (a "cross-talk") among such agonists released following bacteriolysis, is probably the main cause for septic shock and multiple organ failure. It is proposed that a use of bacteriolysis-inducing antibiotics should be avoided in bacteremic patients and particularly in those patients already suspected of developing shock symptoms as these might further enhance bacteriolysis and the release of LPS, LTA and PPG. Furthermore, in additonal to the supportive regimen exercised in intensive care settings, a use of non bacteriolysis-inducing antibiotics when combined with highly sulfated compounds (e.g. heparin, and other clinically certified polysufates) should be considered instead, as these might prevent the activation of the microbial own autolytic systems induced either by highly cationic peptides released by activated phagocytes or by the highly bacteriolytic beta-lactams. Polysulfates might also depress the deleterious effects of the complement cascade and the use of combinations among anti-oxidants ( N-acetyl cysteine), proteinase inhibitors and phospholipids might prove effective to depress the synergistic cytotoxic effects induced by inflammatory agonists. Also, a use of gamma globulin enriched either in anti-LPS or in anti-LTA activities might serve to prevent the binding of these toxins to receptors upon macrophage which upon activation generate inflammatory cytokines. Thus, a use of "cocktails" of anti-inflammatory agents might replace the unsuccessful use of single antagonists proven in scores of clinical trials of sepsis to by ineffective in prolonging the lives of patients. It is enigmatic why the concept, and the publications which support a role for cationic peptides also as potent inducers of bacteriolysis, an arch evil and a deleterious phenomenon which undoubtedly plays a pivotal role in the pathophysiology of post-infectious sequelae, has been consistently disregarded.
Anti-Bacterial Agents↗
Penicillin-induced changes in the cell wall composition of Staphylococcus aureus before the onset of bacteriolysis.
To analyze if chemical cell wall alterations contribute to penicillin-induced bacteriolysis, changes in the amount, stability, and chemical composition of staphylococcal cell walls were investigated. All analyses were performed before onset of bacteriolysis i.e. during the first 60 min following addition of different penicillin G doses. Only a slight reduction of the amount of cell wall material incorporated after penicillin addition at the optimal lytic concentration was observed as compared to control cells. However, the presence of higher penicillin G concentrations reduced the incorporation of wall material progressively without bacteriolysis. Losses of wall material during isolation of dodecylsulfate insoluble cell walls were monitored to assess the stability of the wall material following penicillin addition. Wall material grown at the lytic penicillin concentration was least stable but about 30% of the newly incorporated wall material withstood even the harsh conditions of mechanical breakage and dodecylsulfate treatment. Dodecylsulfate insoluble cell walls were used for chemical analyses. While peptidoglycan chain length was unaffected in the presence of penicillin, other wall parameters were considerably altered: peptide cross-linking was reduced in the wall material synthesized after addition of penicillin; reductions from approx. 85% in controls to about 60% were similar for lytic and also for very high penicillin concentrations leading to nonlytic death. O-acetylation was also reduced after treatment with penicillin; this effect paralleled the occurrence of subsequent bacteriolysis at different drug concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylation↗
A special morphogenetic wall defect and the subsequent activity of "murosomes" as the very reason for penicillin-induced bacteriolysis in staphylococci.
The actual reason for the penicillin-induced bacteriolysis of staphylococci was shown to be the "punching" of one or a few minute holes into the peripheral cell wall at predictable sites. These perforations were the result of the lytic activity of novel, extraplasmatic vesicular structures, located exclusively within the bacterial wall material, which we have named "murosomes". In untreated staphylococci the punching of holes into the peripheral wall is a normal process which follows cross wall completion and represents the first visible step of cell separation. Under penicillin, however, analogous holes are punched by the murosomes at sites of presumptive cell separation even if no sufficient cross wall material had been assembled before at this site (but had rather been deposited at other sites). Consequently, because of the internal pressure of the protoplast, lytic death is the inevitable result of this perforation of the protective peripheral wall. Hence, the real mechanism of penicillin-induced bacteriolysis in staphylococci is considered to be mainly the result of a special morphogenetic wall defect: bacteriolysis is taking place regularly when a cell separation process is no longer preceeded by sufficient cross wall assembly at the correct place. However, hypotheses which are based purely on some variations of overall biochemical processes like total wall enzyme activities or total wall synthesis are not regarded to be sufficient to explain this type of lytic death.
Bacteriolysis↗
Antibody complement-dependent bacteriolysis in experimentally induced pasteurellosis in mice.
Affinity-purified bovine immunoglobulin isotypes were bacteriolytic for Pasteurella haemolytica biotype A, serotype 1 (PHA-1). This bacteriolysis was specific and complement-dependent. The IgM and IgG1 were the most active isotypes in the classic complement cascade. These isotypes also induced bacteriolysis through the alternative complement cascade. The comparative bacteriolytic activities of IgG1 and IgM were equal within each cascade; however, the bacteriolytic activities of IgG1 and IgM were lower in the alternative cascade than in the classical cascade. The IgG2 was more bacteriolytic than IgA in the classic and alternative complement pathways. Bovine immunoglobulins passively protected C57BL/6 mice from experimentally induced pasteurellosis. There were no major differences in the protection among hyperimmune sera, purified IgM, or purified IgG. Mice were protected from PHA-1 by approximately 1.9 micrograms of IgG and 1.2 or 0.1 micrograms of IgM. Elimination of murine complement with cobra venom factor 3 reduced PHA-1 clearance in passively immunized C57BL/6 mice. The protective effect of IgM mediated resistance was highly dependent on an intact complement system. The intact complement cascade was associated with enhanced clearance of PHA-1 from the liver. Although PHA-1 was susceptible to antibody complement-mediated bacteriolysis in vitro, the dependence on an intact complement cascade was not absolute in experimentally induced murine septicemic pasteurellosis.
Animals↗
Monobactam antibiotics in subinhibitory concentrations enhance opsonophagocytosis and serum bacteriolysis in certain Escherichia coli strains.
Capsular polysaccharides are known to protect Gram-negative bacteria from complement-mediated killing and opsonophagocytosis. Monobactam antibiotics selectively inhibit penicillin-binding protein 3 (PBP3), resulting in abnormally structured peptidoglycan, causing defective cell surface structures. The authors studied the influence of subinhibitory concentrations of the monobactam antibiotics aztreonam and carumonam on serum bacteriolysis and opsonophagocytosis of four K-encapsulated and five non-K-encapsulated Escherichia coli strains. It was observed that monobactam antibiotics in subinhibitory concentrations enhanced opsonophagocytosis of the four K-encapsulated and one non-K-encapsulated E. coli strains tested. Opsonophagocytosis of the other four non-K-encapsulated E. coli strains was not enhanced. Serum bacteriolysis studies revealed that of the four K-encapsulated strains tested only one strain showed a significant enhancement of bacteriolysis after treatment with subinhibitory concentrations of monobactam antibiotics. None of the unencapsulated strains showed a significant change in percentage lysis after treatment with either aztreonam or carumonam.
Anti-Bacterial Agents↗
Suppression of penicillin-induced bacteriolysis of staphylococci by some anticoagulants.
Heparinoids and related negatively-charged substances caused suppression of the penicillin-induced bacteriolysis of staphylococci and a higher viability rate. Furthermore, the penicillin-induced release of cell wall material was reduced by these substances. The main reason for this suppression of bacteriolysis was an inhibition of the activity of cell wall autolytic enzymes while the penicillin-specific perturbations of wall morphogenesis were not affected.
Anticoagulants↗
Effect of amplification of the Cap b locus on complement-mediated bacteriolysis and opsonization of type b Haemophilus influenzae.
Amplification of the Cap b locus of Haemophilus influenzae occurs frequently in clinical isolates and has been proposed to be a mechanism by which this organism evades host defense. To determine if amplification of this locus affected complement fixation, in vitro studies to determine complement-mediated bacteriolysis and complement-mediated opsonization of an isogenic set of organisms containing 2, 3, and 4 copies of the Cap b locus were performed. Organisms containing 4 copies of the Cap b locus were significantly more resistant to antibody-dependent, classical complement pathway-directed bacteriolysis than were organisms containing 2 copies. Organisms containing 3 copies of this locus exhibited intermediate susceptibility to lysis. Complement-mediated opsonization of these organisms was assessed by determining the degree of binding of bacteria to murine or human macrophages or to nonphagocytic cells transfected with the genes for human Mac-1, the complement receptor type 3. In all three assay systems, organisms containing 4 copies of the Cap b locus bound less well than did organisms containing 2 copies of this locus. Consistent with their decreased susceptibility to lysis and opsonization, organisms with 4 copies of the Cap b locus fixed less C3 than did organisms containing 2 copies. These data demonstrate that amplification of the Cap b locus is associated with decreased susceptibility to complement-mediated lysis and decreased complement-mediated opsonization and suggest that amplification is used by these pathogens to increase their resistance to complement-dependent host defense mechanisms [correction of mecanisms].
Adult↗
[Correlation between the intensity of spontaneous bacteriolysis and bacterial pollution in superficial waters].
A study on the determination of the intensity of spontaneous bacteriolysis in different samples of water from the hydrographic basin of Lorraine, has led us to propose a new way of expressing the spontaneous bacteriolytic power: PBSG. Its utilization has permitted us to establish correlations between the intensity of spontaneous bacteriolytic power and the degree of bacteriological pollution found in different places in the two rivers, the Moselle and the Meurthe. A very strong correlation has been shown between the rate of global spontaneous bacteriolysis after 6 days and the number of coliforms in the water.
Bacteriolysis↗
Onset of penicillin-induced bacteriolysis in staphylococci is cell cycle dependent.
Synchronously growing staphylococci were treated with "lytic" concentrations of penicillin at different stages of their division cycle. Coulter Counter measurements and light microscopy were used to determine the onset of bacteriolysis. Independent of the stage of the division cycle at which penicillin was added, (i) the cells were always able to perform the next cell division; (ii) the following division, however, did not take place; and (iii) instead, at this time, when the onset of the subsequent cell separation was observed in control cultures, lysis of the penicillin-treated cells occurred. These results support a recent model (P. Giesbrecht, H. Labischinski, and J. Wecke, Arch. Microbiol. 141:315-324, 1985) explaining penicillin-induced bacteriolysis of staphylococci as the result of a special morphogenetic mistake during cross wall formation.
Cell Cycle↗
Protamine and polyarginine bacteriolysis. Similarities in its mechanism with chromatin DNA picnosis.
Protamine and polyarginine had bacteriolytic effects indicating their primary sites of action as being wall components and showing bacterial diversity genetically determined. Shake-incubation was required in producing cell-lysis. Studies on Bacillus subtilis revealed a high polycation multiplicity per cell in lytic event displaying multihit lysing kinetics; bacteriolysis was inhibited by trypsin, pronase, purified polyanionic wall polysaccharide, and by dissociative actions of salt hypermolarities used in isolation of nucleic acids. The inactivation of polycation lytic abilities during bacteriolysis was accompanied by modifications in electrophoretic running of protamine and polyarginine. It is suggested as mechanism of cell-lysis, the multiple zonal surface condensations of polyanionic wall components by basic polypeptides, likely similar with chromatin DNA picnosis. This analogy is discussed.
Anti-Bacterial Agents↗
Neither an enhancement of autolytic wall degradation nor an inhibition of the incorporation of cell wall material are pre-requisites for penicillin-induced bacteriolysis in staphylococci.
In contrast to what has been postulated, penicillin G at its optimal lytic concentration of 0.1 microgram per ml did not lead to a detectable activation of autolytic wall processes in staphylococci in terms of the release of uniformly labelled wall fragments from cells pretreated with the drug for 1 h. Rather a considerable inhibition of this release was observed. A similarly profound inhibition of the release of peptidoglycan fragments occurred when staphylococci pretreated for 1 h with 0.1 microgram penicillin per ml acted as a source of crude autolysins on peptidoglycan isolated from labelled normal cells of the same strain. This clearly demonstrated that the overall inhibition of autolytic wall processes caused by penicillin was mainly due to a decreased total autolysin action rather than to an altered wall structure. Furthermore, no substantial penicillin-induced inhibition of the incorporation of 14C-N-acetylglucosamine into the staphylococcal wall could be observed before bacteriolysis started, i.e., approximately during the first 80 min of penicillin action. These results are not consistent with any of the models hitherto proposed for the action of penicillin.
Bacteriolysis↗
Heterogeneity in the complement-dependent bacteriolysis within the species of Borrelia burgdorferi.
Sixteen Borrelia burgdorferi strains, including all three species, were compared in a colorimetric bactericidal assay for their ability to escape the complement-dependent bacteriolysis on incubation in normal human serum free of specific antibodies (NHS). The species B. afzelii was found to be serum resistant (EB1, EB3, FEM1, FEM2, Pko), whereas strains of the species B. garinii were found to be serum sensitive (1/B29, G1, G2, PSth, PBr, PTrob). Six strains, mainly B. burgdorferi sensu stricto, were only partially sensitive (Z25, 297, B31, PKa-I, PBi). All strains activated the complement cascade in NHS, whereas only four strains (G1, G2, PBr, PSth) could activate complement in the presence of EGTA-Mg. After complement activation, covalently bound C3 fragments (C3b, iC3b) were detected on serum-sensitive as well as serum-resistant borrelial strains. Heterogeneity, however, was observed between serum-resistant and serum-sensitive strains with respect to deposition of C6 and C9. Whereas serum-sensitive strains were strongly positive for C6 and C9 and were, therefore, killed by the terminal complement complex (TCC), serum-resistant strains were devoid of C6 and C9 on their cell surface. The serum resistance may, therefore, be due to an absent or only transient formation of TCC on the bacterial surface.
Bacteriolysis↗
Concurrent assessment of inner and outer membrane permeabilization and bacteriolysis in E. coli by multiple-wavelength spectrophotometry.
We developed a dual wavelength spectrophotometric assay that permitted beta-lactamase and beta-galactosidase activities to be measured concurrently in a single sample. We also constructed a target cell, E. coli ML-35p, that was substantially cryptic for its periplasmic beta-lactamase and cytoplasmic beta-galactosidase unless outer membrane (beta-lactamase) or inner membrane (beta-galactosidase) permeabilization occurred. By applying the spectrophotometric assay to whole target cells, we could ascertain the kinetics of inner and outer membrane permeabilization by biological agents, including serum, polymyxin B and mellitin. By monitoring the reactions at an additional wavelength, we could also follow the kinetics of serum-mediated bacteriolysis. These experiments illustrate the principle of multiple wavelength spectrophotometry and provide examples of its use to monitor and dissect the action of biological agents on a gram-negative bacterium.
Bacteriolysis↗
The effect of leukocyte hydrolases on bacteria. III. Bacteriolysis induced by extracts of different leukocyte populations and the inhibition of lysis by macromolecular substances.
The lysis of 14C-labeled bacteria by hydrolases of human and rabbit leukocytes was studied in vitro. While Staphylococcus albus, Streptococcus faecalis, and Streptococcus mutans were highly susceptible to lysis, Staphylococcus auresus was intermediate in its susecptibility to lysis by the leukocyte enzymes. Group A Streptococcus, Listeria monocytogenes, Shigella flexneri, Escherichia coli, and Mycobacterium smegmatis were very resistant to degradation by these enzymes. The lytic activity of leukocyte lysates from human and rabbit blood was probably due to acid hydrolases of polymorphonuclear leukocytes. Extracts of human blood monocytes and of rabbit peritoneal and lung macrophages were less lytic for the bacteria tested. Lymphocytes and platelet extracts were not bacteriolytic. The lytic effect of the leukocyte lysates was not inhibited by KCN or sodium azide, but was abolished to a large extent by cationic polyelectrolytes such as protamine sulfate, histone and leukocyte cationic proteins, and poly-lysine, as well as by the anionic polyelectrolytes such as heparin, chondroitin sulfate, DNA, carrageenin, alginate sulfate, dextran sulfate, and ploy-L-glutamic acid. Other potent inhibitors of bacteriolysis were trypan blue, congo red, phosphatidic acid, normal immunoglobulins, and components of streptococcal cell wall.
Animals↗