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J Wecke

Publications and source records attributed to J Wecke.

35 records · Page 2Linked to original sources
PubMed1992

Fan-shaped ejections of regularly arranged murosomes involved in penicillin-induced death of staphylococci.

Electron microscopic research into the murosomes of staphylococci has shown that the number of murosomes involved in penicillin-induced death varies depending on the experimental conditions employed. With 0.1 micrograms of penicillin G per ml, only 1 of a total of about 20 murosomes, the "killing murosome," completely perforated the pressure-stabilized peripheral cell wall during a three-step process. This strictly localized event was mainly attributed to a mechanical effect being comparable to the process of aneurysm formation. Wall perforation was also considered to mark the very moment of penicillin-induced death ("nonlytic killing event"), while bacteriolysis started only postmortem. By varying the osmolarity of the growth medium, the number of murosomes involved in penicillin-induced killing increased considerably, which resulted in the ejection of a fan-shaped row of murosomes at the second division plane. These data are compatible with the finding that, in untreated or chloramphenicol-treated staphylococci, the activation of the murosomes resulted in (i) the formation of regularly arranged "blebs" on the cell surface, containing traces of disintegrated wall material, and (ii) the subsequent liberation of the murosomes lying underneath, leaving behind their former sites in the peripheral wall as a row of regularly arranged "pores" in every division plane. The number, distribution, and positioning of these blebs corresponded with those of the pores and the original murosomes. The significance of wall autolysins liberated from the first division plane for penicillin-induced wall perforation at the second division plane is discussed.

Cell Division↗
PubMed1992

The modulation of the bacteriolytic effect of beta-lactam antibiotics by non-antibiotics.

The addition of cationic proteins such as lysozyme, ribonuclease and cytochrome C enhanced the beta-lactam-induced bacteriolysis of staphylococci measured as release of wall label or by optical density. The treatment of staphylococci with penicillin plus cytochrome C resulted in a reduced viability of bacteria compared with those treated with penicillin alone. The wall autolysis and the penicillin-induced bacteriolysis of staphylococci were enhanced by the lysosomal enzyme cathepsin C. The penicillin-induced bacteriolysis was also enhanced by the D-amino acids D-alanine and D-methionine, while the comparable L-amino acids did not reveal any activity. On the other hand, some polyanionic substances were able to suppress the penicillin-induced bacteriolysis. Radiochemical and electron microscopic studies revealed the participation of bacterial wall autolysins in the first steps of degradation processes of staphylococcal walls within murine bone marrow-derived macrophages.

Amines↗
PubMed1991

Macrophages produce somnogenic and pyrogenic muramyl peptides during digestion of staphylococci.

Muramyl peptides have a variety of biological effects in mammals, including enhancement of the immune response, sleep, and body temperature. Although mammals lack biosynthetic pathways for muramyl peptides, they are found in mammals and are well known as components of bacterial cell walls. This suggests that phagocytic mammalian cells digest bacterial cell walls and produce biologically active muramyl peptides. Staphylococcal cell walls were radioactively labeled during growth of the bacteria. During the digestion of these radiolabeled bacteria, murine bone marrow macrophages produced low-molecular-weight substances that coeluted chromatographically with the radioactive cell wall marker. Further separation of these substances using reversed-phase high-performance liquid chromatography resulted in the isolation of substances with high specific biological activity. Intracerebroventricular injection of rabbits with these substances induced an increase in slow-wave sleep and body temperature and a suppression of rapid-eye-movement sleep. The characteristics of the biological responses and the chromatographic behavior of the active components are consistent with those of muramyl peptides. The ability of macrophages to tailor muramyl peptides from peptidoglycan may provide an amplification step for the immune response. Muramyl peptides released by macrophages may also act as mediators for various facets of the acute phase response elicited by bacterial infections such as fever and sleep.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1990

Reduction of wall degradability of clindamycin-treated staphylococci within macrophages.

Clindamycin treatment of Staphylococcus aureus caused a remarkable thickening of the bacterial cell wall and made the bacterial wall much more resistant against lytic enzymes within bone marrow-derived macrophages as revealed by electron microscopy and radiolabeling experiments. This reduced wall degradability resulted from an increased number of O-acetyl groups in the murein. Furthermore, such clindamycin-treated bacteria were ingested by adherent bone marrow-derived macrophages at a higher rate than untreated bacteria. The medical aspects of these results are discussed.

Animals↗
PubMed1990

Inhibition of the bacteriolytic effect of beta-lactam-antibiotics on Staphylococcus aureus by the polyanionic drugs suramin and Evans Blue.

The anionic polyelectrolytes suramin and Evans Blue inhibited different autolytic systems involved in wall growth and wall turnover of growing staphylococci and in wall autolysis of resting bacteria. Moreover, both substances lowered the beta-lactam-induced pre-lytic release of cytoplasmic constituents from staphylococci, and inhibited the beta-lactam-induced bacteriolysis as well as the loss of viability. The protective effects of these sulfonated drugs against bacteriolysis were also monitored by electron microscopy. Some medical implications of our results are discussed.

Anti-Bacterial Agents↗
PubMed1987

Trimethoprim-induced structural alterations in Staphylococcus aureus and the recovery of bacteria in drug-free medium.

Bacteriostatic concentrations of trimethoprim, which possibly acts as a DNA-inhibitor, induced the swelling of staphylococci and affected their cell walls, their cytoplasmic membrane and part of their autolytic wall system. Trimethoprim proved to be the first growth-inhibiting drug that did not induce the formation of thickened cell walls in staphylococci. An ultrastructurally important effect of trimethoprim treatment was the appearance of mesosome-like structures which were not fixation artefacts. Additionally, trimethoprim led to the formation of incomplete cross walls, while cross wall initiation continued virtually unaffected. After removal of trimethoprim, extremely fast growth restoration occurred with the formation of new cell wall material underlying the old wall. Afterwards, the old wall material was disintegrated by autolytic processes.

Bacteriolysis↗
PubMed1987

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↗
PubMed1986

Inhibition of wall autolysis of staphylococci by sodium polyanethole sulfonate "liquoid".

Liquoid (polyanethole sulfonate) was neither capable of influencing the growth nor the viability of staphylococci. But liquoid induced a suppression of the activity of different autolytic wall systems of normally growing staphylococci, i.e., autolysins which participate in cross wall separation as well as autolysins which are responsible for cell wall turnover. Additionally, the lysostaphin-induced wall disintegration of staphylococci was inhibited by liquoid. However, no indication could be found for a direct inhibition of lytic wall enzymes by liquoid; rather an interaction of liquoid with the target structure for the autolytic wall enzymes, the cell wall itself, was postulated. On the basis of the experimental data with the teichoic acid- mutant S. aureus 52A5 the sites of wall teichoic acid were supposed to be an important target for the binding of liquoid to the staphylococcal cell wall.

Bacteriolysis↗
PubMed1985

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↗
PubMed1985

Persistence of staphylococcal cell-wall components in inflammatory sites may be due to the modulation by sulphated polyelectrolytes of autolytic wall enzymes: a working hypothesis.

The interaction of leucocytes with Staphylococcus aureus results in killing of the bacterial cells, but large portions of the bacterial cell walls persist apparently phagocytic cells for long periods. The mechanisms of biodegradation of staphylococci by leucocyte factors have shown that degradation of cell walls in vitro may be the result of the activation, by leucocyte kationic proteins, of the bacterial autolytic wall enzymes that are responsible for degrading the cell walls from within. This process is markedly inhibited by sulphated polysaccharides like dextran sulphate, by heparin, or by polyanetholesulfonate (liquoid). These anionic polyelectrolytes have also been shown to inhibit the lysis of staphylococci treated with bacteriolytic concentrations of penicillin G. Staphylococci injected intraarticularly into the knee joint of rats underwent massive plasmolysis, but structures compatible with cell walls (peptidoglycan) persisted within macrophages in the inflammatory sites, for long periods. It is postulated that the inability of leucocytes to degrade staphylococcal cell-wall components may be the result of the interference, by anionic polyelectrolytes likely to accumulate in the inflammatory sites, with the activation of the autolytic systems. Alternatively, anionic polyelectrolytes may coat the bacterial cells and interfere with the binding of the autolytic enzymes with their corresponding substrates.

Animals↗
PubMed1982

Cell wall degradation of Staphylococcus aureus by lysozyme.

In contrast to former findings lysozyme was able to attack the cell walls of Staphylococcus aureus under acid conditions. However, experiments with 14C-labelled cell walls and ribonuclease indicated that, under these conditions, lysozyme acted less as an muralytic enzyme but more as an activator of pre-existing autolytic wall enzymes. Electron microscopic studies showed that under these acid conditions the cell walls were degraded by a new mechanism (i.e. "attack from the inside"). This attack on the cell wall started asymmetrically within the region of the cross wall and induced the formation of periodically arranged lytic sites between the cytoplasmic membrane and the cell wall proper. Subsequently, a gap between the cell wall and the cytoplasmic membrane resulted and large cell wall segments became detached and suspended in the medium. The sequence of lytic events corresponded to processes known to take place during wall regeneration and wall formation. In the final stage of lysozyme action at pH 5 no cell debris but "stabilized protoplasts" were to be seen without detectable alterations of the primary shape of the cells. At the same time long extended ribbon-like structures appeared outside the bacteria. The origin as well as the chemical nature of this material is discussed. Furthermore, immunological implications are considered.

Cell Wall↗
PubMed1977

The demonstration of the existence of an interlayer between the cytoplasmic membrane and the cell wall proper of staphylococci.

By disintegration of the cell wall of staphylococci a definite interlayer located between the cytoplasmic membrane and the cell wall proper could be demonstrated for the first time (MW-interlayer). This MW-interlayer contains a sort of "cloddy" material in which clusters of embedded ring-like disks are hexagonally arranged in a crystal-like manner. The ring-like disks, approximately 40 A in diameter and with center-to-center spacings of approximately 75 A, -lie in direct contact either with a rhombically arranged fibrillar network of the outer parts of the cytoplasmic membrane or they themselves are part of (or interconnected by) such an apparently rhombical network. The crystal-like arranged ring-like disks of the interlayer between the cytoplasmic membrane and the cell wall shall be called MW-particles in order to differentiate them from intramembrane particles and particles on the outer surface of the cell wall. At present, nothing more than speculation on the function of the MW-particles located within the space where final processes of the cell wall polymerization are taking place is possible.

Cell Membrane↗
PubMed1976

Treponema pallidum in early syphilitic lesions in humans during high-dosage penicillin therapy. An electron microscopical study.

The alterations of early syphilitic infection occuring in the course of high dosage penicillin (120 mega IU, 36 h) as clinical experimental trial has been studied both from the clinical and the electron microscopical views. By electron microscopical studies, findings revealing the localization and the status of treponemes before and during penicillin treatment could be established. Before treatment started, the majority of treponemes was of intercellular localization. In the course of treatment various forms of destruction could be differentiated. The most striking change in the host tissue after 7-8 h of penicillin therapy was an elimination of treponemes by penetrating phagocytes. 24 h after the beginning of treatment, treponemes could not be demonstrated any more. The clinical and serological findings after the high dosage penicilline will produce results comparable to those of conventional therapie.

Adult↗
PubMed1975

Demonstration of cytoplasmic actomyosin fibrils by the freeze-etching technique.

Cytoplasmic actomyosin fibrils of Physarum polycephalum were demonstrated by the freeze-etching technique. Within the fibrils the electron micrographs reveal 40-80 A thick filaments presumably representing F-actin. Thicker filaments (myosin) could not be detected. To avoid freezing artefacts, a pretreatment of the living material with 50% sucrose was necessary. The influence of freeze-protecting agents upon the fine structure of cytoplasmic actomyosins and the resulting difficulties in the investigation of constituents of the groundplasm with the freeze-etching technique are discussed.

Cytoplasm↗