Search PubMed⌕ Search

Biomedical subjects

J Verhoef

Publications and source records attributed to J Verhoef.

At least 487 records · Page 27Linked to original sources
PubMed1985

Activation of polymorphonuclear leukocytes by spermatozoa.

Human spermatozoa activated human polymorphonuclear leukocytes (PMN) in the presence of serum. Activation of PMN was studied by measuring the emission of chemiluminescence by the PMN. The amount of chemiluminescence emitted depended on the number of spermatozoa and the serum concentration, and the presence of antibody or complement. Spermatozoa were able to activate PMN in the presence of heat-inactivated serum (only antibody, no complement), serum obtained from a patient with agammaglobulinemia (without antibodies and only complement as opsonin), and in MgEGTA agammaglobulinemic serum (only the alternative pathway of complement intact). In the presence of heat-inactivated agammaglobulinemic serum no significant chemiluminescence was observed. It was concluded that spermatozoa activate the alternative pathway of complement. Dead spermatozoa were more able to activate PMN than viable spermatozoa.

Adolescent↗
PubMed1985

Do quinolones really augment the antifungal effect of amphotericin B in vitro?

The minimum inhibitory concentrations (MICs) for amphotericin B and the quinolones norfloxacin and ciprofloxacin against 30 clinical isolates of Candida albicans were determined in various liquid media. Interaction studies were carried out to investigate a possible synergistic action of the quinolones on the antifungal effect of amphotericin B. No interaction between the drugs studied was observed in any of the media used.

Amphotericin B↗
PubMed1985

Endotoxic effects of peptidoglycan.

Peptidoglycans (PG) are cell wall fragments of gram-positive bacteria. The effect of PG on blood pressure, circulating leukocytes, and platelets was studied in a rat model. PG was able to decrease blood pressure and to induce leukopenia and thrombocytopenia. In vitro PG affected leukocyte function and was able to activate the contact activating system.

Animals↗
PubMed1984

Differences in the effect of arachidonic acid on polymorphonuclear and mononuclear leukocyte function.

Incubation of human polymorphonuclear leukocytes with arachidonic acid resulted in a stimulation of the oxidative metabolism of the cells. Upon stimulation with 80 microM arachidonic acid, neutrophils (5 X 10(6) cells/ml) produced superoxide (53 +/- 8 nmol/5 X 10(6) cells per 15 min), generated chemiluminescence (1211 100 +/- 157 000 cpm) and consumed oxygen (20 +/- 1 nmol/10(6) cells per 5 min). The stimulation of the cell metabolism could be reduced 40-60% by prior incubation of the cells with 10 microM indomethacin. Incubating polymorphonuclear leukocytes with arachidonic acid also resulted in a diminished chemotaxis towards an attractant, a decreased uptake of opsonized staphylococci and aggregation of the cells. This may be due to inhibitory products of arachidonic acid metabolism and toxic oxygen species produced during stimulated oxidative metabolism. The effects of arachidonic acid are specific for neutrophils, as mononuclear phagocytes only produced 17 +/- 8 nmol superoxide/5 X 10(6) cells per 15 min and generated 27 000 +/- 15 000 cpm chemiluminescence when stimulated with 80 microM arachidonic acid. When monocytes and neutrophils were stimulated with particles such as opsonized staphylococci, the amount of superoxide produced, oxygen consumed and chemiluminescence generated were similar. The phagocytic activity of the monocytes was also not affected by prior incubation with arachidonic acid. We conclude that in contrast to monocytes, neutrophil metabolism can be stimulated with arachidonic acid and this stimulation resulted in a decreased phagocytic activity of these cells.

Arachidonic Acid↗
PubMed1984

Host-parasite interaction in serious infections due to gram-negative bacteria.

Gram-negative rods such as Enterobacteriaceae and Pseudomonadaceae are normal habitants of the digestive tract. However, if defense mechanisms of the host are compromised by underlying diseases such as malignant neoplasms, renal insufficiency, extensive traumata, or immunosuppressive therapy, invasion of the blood-stream can occur. Gram-negative septicaemia is associated with high morbidity and mortality, despite intensive care and administration of potent antibiotics. A central role in the pathophysiology of life-threatening bacteriaemia is attributed to endotoxin, a constituent of the gram-negative cell wall. This paper reviews current concepts of septic shock, the acquisition of gram-negative bacteraemia and the role of endotoxin. It also deals with a new approach to prevention and control of severe gram-negative infections using serotherapy based on the structure of endotoxin.

Animals↗
PubMed1984

New aspects of staphylococcal infections: emergence of coagulase-negative staphylococci as pathogens.

In contrast to the well-established pathogen Staphylococcus aureus, the coagulase-negative staphylococci, formerly collectively called S. epidermidis, were until recently regarded as harmless commensals. During the last two decades, however, the coagulase-negative staphylococci have clearly emerged as pathogens in patients carrying artificial devices, such as prosthetic heart valves, hip prostheses and cerebrospinal fluid shunts, and in patients with compromised host defenses such as premature neonates and cancer and transplant patients. The present paper reviews current insights on classification, bacteriology, pathogenic potential and virulence factors of coagulase-negative staphylococci. In addition, the role of host defense factors in resistance to staphylococcal infection is summarized as well as the main features of the clinical syndromes in which coagulase-negative staphylococci are involved.

Antibodies, Bacterial↗
PubMed1984

Enhancement of human natural killer cell activity by subcellular components of Toxoplasma gondii.

The ability of sonicates and subcellular fractions of the intracellular parasite Toxoplasma gondii to enhance in vitro human natural killer (NK) cell activity was examined. Incubation of nylon-wool-non-adherent human peripheral blood lymphocytes (PBL) with sonicates of T. gondii for 18-72 hr resulted in increased NK activity against an NK-sensitive, as well as an insensitive, target cell. Single-cell assays revealed that augmentation of NK activity was not due to an increased binding of K562 target cells to effector cells. Differential centrifugation studies indicated that NK-augmenting activity was distributed in membrane-enriched and cytoplasmic fractions. This activity was found to be resistant to treatment with ribonuclease (RNase) and deoxyribonuclease (DNase), but susceptible to proteolysis. Antibodies present in the serum of humans infected with Toxoplasma blocked the NK cell-augmenting effect of the membrane-enriched fractions. Enhancement of NK activity by PBL incubated with Toxoplasma sonicate was accompanied by a concomitant increase in interferon (IFN), but not of interleukin 2 (IL-2), levels in supernatants of the cell cultures.

Adult↗
PubMed1984

Functional defects in phagocytic cells from patients with iron overload.

Phagocytic functions were studied in patients with iron overload. Phagocytosis of radiolabelled opsonised Staphylococcus aureus by mononuclear (MN) leucocytes and polymorphonuclear (PMN) leucocytes was measured in 15 and 16 patients, respectively. The intracellular killing capacity of MN and PMN leucocytes of seven and nine patients, respectively, and chemotaxis of PMN leucocytes of eight patients, were assessed also. These cellular functions were compared with phagocytic functions of controls tested on the same day, and with the normal ranges of phagocytic cell functions obtained with MN and PMN leucocytes from 48 and 59 healthy donors, respectively. One or more phagocytic functions were impaired in 62.5 per cent of the patients. Comparison of the various phagocytic functions in patients and simultaneously tested controls showed a significant decrease of the mean phagocytic capacity of the patients' MN and PMN leucocytes (P less than 0.015 and P less than 0.03, respectively), as well as the mean bactericidal activity of the MN leucocytes (P less than 0.05) and the mean chemotactic responsiveness of the PMN leucocytes (P less than 0.025). Patients with excess iron must be regarded as compromised hosts, not only because of the increased availability of iron for bacterial growth, but also because of the associated functional impairment of monocytes and granulocytes.

Adolescent↗
PubMed1984

Degradation of Escherichia coli chromosomal and plasmid DNA in serum.

Incubation of serum-sensitive [3H]thymidine labelled Escherichia coli PC2166 (RSF1030) and E. coli AM1281 (pBR322) harbouring small plasmids (mol. wt 5.5 X 10(6) and 2.6 X 10(6] in serum resulted in killing of 99.9% of the bacteria within 15 min and in the release of 85% of the radioactivity into the medium after 1 h incubation. The fate of chromosomal and plasmid DNA during incubation of the bacteria in serum was analysed by measurement of the amount of DNA-associated radioactivity, by TCA precipitation, by agarose gel electrophoresis and by the capacity of DNA to transform competent acceptor bacteria. Chromosomal DNA and high molecular weight plasmid DNA were rapidly degraded after 1 h incubation of bacteria in serum. However, low molecular weight plasmid DNA was virtually unaffected and remained physicochemically as well as biologically intact during up to 4 h of incubation of bacteria in serum.

Blood Bactericidal Activity↗
PubMed1984

Effect of human polymorphonuclear and mononuclear leukocytes on chromosomal and plasmid DNA of Escherichia coli. Role of acid DNase.

Phagocytosis and killing by polymorphonuclear and mononuclear leukocytes are important host resistance factors against invading microorganisms. Evidence showing that killing is rapidly followed by degradation of bacterial components is limited. Therefore, we studied the fate of Escherichia coli DNA following phagocytosis of E. coli by polymorphonuclear and mononuclear leukocytes. [3H]thymidine-labeled, unencapsulated E. coli PC2166 and E. coli 048K1 were incubated in serum, washed, and added to leukocytes. Uptake and killing of the bacteria and degradation of DNA were measured. Although phagocytosis and killing by mononuclear leukocytes was less efficient than that by polymorphonuclear leukocytes, only mononuclear leukocytes were able to degrade E. coli PC2166 DNA. Within 2 h, 60% of the radioactivity added to mononuclear leukocytes was released into the supernate, of which 40% was acid soluble. DNA of E. coli 048K1 was not degraded. To further analyze the capacity of mononuclear leukocytes to degrade E. coli DNA, chromosomal and plasmid DNA was isolated from ingested bacteria and subjected to agarose gel-electrophoresis. Only chromosomal DNA was degraded after phagocytosis. Plasmid DNA of E. coli carrying a gene coding for ampicillin resistance remained intact for a 2-h period after ingestion, and was still able to transform recipient E. coli cells after this period. Although we observed no DNA degradation during phagocytosis by polymorphonuclear leukocytes, lysates of both polymorphonuclear and mononuclear leukocytes contained acid-DNase activity with a pH optimum of 4.9. However, the DNase activity of mononuclear leukocytes was 20 times higher than that of polymorphonuclear leukocytes. No difference was observed between DNase activity from polymorphonuclear and mononuclear leukocytes from a chronic granulomatous disease patient with DNase activity from control polymorphonuclear and mononuclear leukocytes.

Animals↗
PubMed1984

Interaction between human polymorphonuclear leucocytes and Staphylococcus aureus in the presence and absence of opsonins.

Phagocytosis of Staphylococcus aureus by human polymorphonuclear leucocytes (PMN) in the presence and absence of opsonins was studied with an assay which allows interaction between PMN and bacteria on a surface. The kinetics of uptake, the activity of the metabolic burst, and the degranulation during phagocytosis of opsonized and unopsonized bacteria were compared. Uptake of unopsonized S. aureus proceeded at a slower rate, but unopsonized staphylococci induced metabolic activity and degranulation in the PMN to the same extent as opsonized bacteria. Treatment of PMN with a metabolic inhibitor (2-deoxy-D-glucose) or with an inhibitor of microfilament function (cytochalasin B) totally inhibited the capacity of PMN to ingest unopsonized S. aureus, whereas uptake of opsonized bacteria was much less affected. Treatment of the PMN with pronase prevented uptake of unopsonized bacteria, but had no effect on the uptake of opsonized bacteria. Uptake was not inhibited by mannose. Recognition of S. aureus by the PMN was not dependent on the presence of the cell wall components protein A or teichoic acid. The presence of a capsule inhibited uptake.

Cell Wall↗
PubMed1984

Aggregation of human polymorphonuclear leucocytes during phagocytosis of bacteria.

The process of aggregation of human polymorphonuclear leucocytes (PMN) during the uptake of bacteria was studied. Radiolabelled S. aureus were opsonized in different sera, washed, resuspended in buffer and added to the PMN. Uptake of the bacteria and aggregation of the PMN were measured simultaneously. Maximal aggregation occurred within 6 min, when 5 X 10(6) PMN had phagocytosed 2.5 X 10(8) S. aureus. Also the effects of serum concentrations and different sera for opsonization of the bacteria on PMN aggregation were studied. Despite normal uptake, aggregation of PMN was low when bacteria were opsonized in complement-deficient sera. Furthermore when PMN were treated with pronase to inactivate complement receptors on the cell surface of the PMN, and bacteria preopsonized in immune serum were added, no change in uptake occurred, although the degree of aggregation halved compared to control PMN. So, interaction between the bacteria and the complement receptor of the PMN cell membrane is needed for triggering the process of aggregation. By using dansylcadaverin and diphenylamine to modulate lysosomal enzyme release, azide or PMN from a chronic granulomatous disease patient to study the effect of the formation of oxygen species, and theophylline, DB-cAMP or 8 Br-cAMP to increase cAMP levels, it was concluded that aggregation of PMN during phagocytosis was not dependent on oxygen metabolism, degranulation or cAMP levels of PMN.

Adult↗
PubMed1984

Effects of lysosomotropic amines on human polymorphonuclear leucocyte function.

Lysosomotropic agents interfere with lysosome function. We studied the effects of the lysosomotropic amines: lidocaine, diphenylamine and dansylcadaverine on several functions of human polymorphonuclear leucocytes (PMN): enzyme release, phagosome-lysosome fusion, superoxide anion generation upon stimulation with opsonized bacteria, and phagocytosis and killing of opsonized Staphylococcus aureus. Lidocaine depressed all cellular functions tested. Diphenylamine reduced enzyme release and phagosome-lysosome fusion in phagocytosing PMN. This was accompanied by an increase in superoxide anion generation. Dansylcadaverine enhanced enzyme release and phagosome-lysosome fusion, and reduced superoxide anion generation. Neither of these two agents influenced bacterial uptake; bacterial killing was impaired only in dansylcadaverine treated cells. Cadaverine, an analogue that does not penetrate cells, had no effect on any of the functions tested.

Amines↗
PubMed1984

Deferoxamine enhances phagocytic function of human polymorphonuclear leukocytes.

Inhibition of the iron-mediated generation of toxic oxygen species by polymorphonuclear leukocytes (PMN) might prevent oxidative damage and thus enhance phagocytic function of PMN. To investigate this point, we studied the effect of the specific iron chelator, deferoxamine, on the antibacterial function of PMN. PMN were incubated for 20 hr with various concentrations of deferoxamine at 37 degrees C in medium containing 0.54 microM endogenous iron. The cells were then washed, and the phagocytic cell function was assessed. The results were compared with those for control PMN preincubated for 20 hr without deferoxamine, and those of nonincubated PMN. Compared with that of control PMN, the uptake of radiolabeled Staphylococcus aureus by PMN treated with 1 microM-1 mM deferoxamine was, on average, 10%-20% higher. This effect was not observed when iron-saturated deferoxamine (DFO) was used. Bacterial uptake was similarly increased in nonpreincubated PMN or PMN preincubated for 20 hr at 4 degrees C instead of 37 degrees C. The intracellular killing capacity of both deferoxamine-treated and control PMN exceeded 90%. PMN incubated for 20 hr at 37 degrees C with DFO not only phagocytosed more bacteria than control cells, but were also capable of killing the greater number of bacteria ingested. This increased activity of deferoxamine-treated PMN was accompanied by enhanced generation of chemiluminescence and production of superoxide during phagocytosis of S. aureus. These findings indicate that deferoxamine may enhance the antibacterial activity of PMN by protecting the cells against damage by iron-mediated generation of toxic oxygen metabolites in resting PMN.

Blood Bactericidal Activity↗
PubMed1984

Effect of iron (III) in the presence of various ligands on the phagocytic and metabolic activity of human polymorphonuclear leukocytes.

FeCl3 or Fe(III) that attached to chelating ligands such as citrate or nitrilotriacetic acid (NTA) at a molar ratio of 1:1 had a toxic effect on PMN. Uptake of radiolabeled Staphylococcus aureus by PMN, preincubated for 2 hr at 37 degrees C in a medium containing Fe(III)-citrate or Fe(III)-NTA, was significantly lower than that of control PMN preincubated without excess iron (p less than 0.002). However, at a 1:2 molar ratio of Fe(III) to citrate or NTA, the iron was not toxic. In contrast, the iron-liganding molecules transferrin and deferoxamine protected the PMN against the noxious effect of iron at concentrations just high enough to sequester all the iron. Fe(III) increased the generation of luminol chemiluminescence by stimulated PMN, whereas the oxygen consumption of the cells was not altered in the presence of Fe(III); this suggests a catalytic effect of iron on the production by PMN of oxygen metabolites at some step beyond the formation of superoxide. No effect of iron was observed when the incubation was performed at 4 degrees C, nor when an oxygen-radical scavenger such as thiourea, mannitol, or catalase was present in the incubation medium. Also, Fe(III) had much less effect on the phagocytic function of PMN of a patient with chronic granulomatous disease. The results indicate that the Fe(III)-induced defect in the phagocytic capacity of PMN depends on the nature and the concentration of the ligand attached to the iron ion, and also suggest that the noxious effect of iron on the PMN function is a result of its ability to catalyze the generation of toxic oxygen species by these cells.

Blood Bactericidal Activity↗
PubMed1983

Bacterial cell wall components decrease the number of guinea-pig lung beta-adrenoceptors.

Infections of the deeper respiratory airways can contribute to the progression of chronic asthmatic bronchitis. In the present report a number of microorganisms affecting the number of beta-adrenoceptors in guinea-pig lung homogenates are described. Haemophilus influenzae, Streptococcus pneumoniae, Bordetella pertussis and Escherichia coli O111B4 induced a significant decrease of the number of beta-adrenoceptors (by approximately 20%). Staphylococcus aureus, influenza A virus and Escherichia coli J5 were not active. These data point to a common factor shared by gram-negative bacilli; i.e. endotoxin. Purified endotoxin of E. coli O111B4 also decreased the number of beta-adrenoceptors, while E. coli J5-LPS did not. This suggests that neutral polysaccharides of bacterial cell walls, especially those in the 'O'-antigenic side chain of gram-negative endotoxins may be responsible for the decrease of beta-adrenoceptor number and therefore contribute to the pathogenesis of chronic asthmatic bronchitis. Intact endotoxin seems to be necessary since neither the isolated lipid nor the polysaccharide part of E. coli O111B4 LPS affected the number of beta-adrenoceptors in the lung.

Animals↗
PubMed1983

Inhibition of bacterial multiplication by the iron chelator deferoxamine: potentiating effect of ascorbic acid.

Since iron is essential for the multiplication of microorganisms, the effect of the iron chelator deferoxamine, with or without ascorbic acid, on the growth of 43 strains of Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Alcaligenes faecalis, Neisseria meningitidis and species of Salmonella, Enterobacter, Pseudomonas and Providencia, was investigated with the use of an automated turbidimeter. Addition of deferoxamine (25-400 micrograms/ml) to the incubation medium was inhibitory in a dose-dependent fashion. At concentrations between 200-400 micrograms/ml, growth was about 25% lower than control values. However, when ascorbic acid (100 micrograms/ml) was added to the culture medium, this antimicrobial activity of deferoxamine was significantly increased to on average 75% of the control value (p less than 0.05). Ascorbic acid alone had no bacteriostatic properties. Growth in the presence of 200 micrograms/ml deferoxamine combined with 100 micrograms/ml ascorbic acid was significantly lower than that in control media without additions (p less than 0.001). Addition of ferric citrate to the culture medium at a concentration sufficient to saturate all of the deferoxamine with iron, abolished the growth inhibiting effect of deferoxamine. The results provide evidence that deferoxamine is bacteriostatic due to its capacity to deplete iron which would otherwise be used for bacterial multiplication, and that ascorbic acid enhances this antibacterial property of deferoxamine.

Alcaligenes↗