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J Verhoef

Publications and source records attributed to J Verhoef.

At least 451 records · Page 25Linked to original sources
PubMed1986

Measurement of antibody-mediated binding of human polymorphonuclear leukocytes to HSV-1 infected anchorage fibroblasts.

A method for the quantitation of effector cell binding to anchorage fibroblast monolayers infected with HSV-1 is described. Human peripheral blood polymorphonuclear leukocytes (PMN) as effector cells were labeled with chromium-51. Fetal human lung fibroblasts were grown to confluency in microtiter plates, infected with HSV-1 and loaded with anti-HSV antibody. The amount of radiolabeled PMN adhering to the monolayer was determined after appropriate incubation and washings. The effector binding assay was shown to be dependent on specific anti-HSV antibodies, antibody concentration, HSV viral expression, and inoculation time. This assay system is especially useful for the evaluation of effector to target cell conjugate formation when applied to anchorage target cells.

Antibodies, Viral↗
PubMed1986

Human polymorphonuclear leukocytes release leukotriene B4 during phagocytosis of Staphylococcus aureus.

We studied release of leukotriene B4 (LTB4) by human polymorphonuclear leukocytes (PMNs) during phagocytosis of staphylococci in the presence or absence of arachidonic acid. The 12 X 10(7) PMNs incubated with 3 X 10(9) opsonized S. aureus and 50 microM arachidonic acid released 1.45 +/- 0.42 nmol LTB4. No LTB4 was detected after stimulation of PMNs with S. aureus or arachidonic acid by themselves. However, by increasing the concentration of arachidonic acid to 200 or 400 microM, 1.22 +/- 0.45 and 1.98 +/- 0.49 nmol LTB4, respectively, was released by PMNs. The effect of different bacteria-PMN ratios on LTB4 production was also studied. LTB4 varied from 0.3 to 2.0 nmol when bacteria/PMN ratios increased from 5 to 50 (respectively) in the presence of 50 microM arachidonic acid. Thus, phagocytizing PMNs produce LTB4 in the presence of arachidonic acid, and its production is dependent on the number of bacteria phagocytized.

Arachidonic Acids↗
PubMed1986

Complement activating and opsonic capacity of monoclonal antibodies raised against Escherichia coli O111 and its rough mutant J5.

Six monoclonal antibodies raised against Escherichia coli O111 and against its rough mutant J5 (chemotype Rc) were studied. One IgG2A, one IgM anti-J5, and one IgG2A anti-O111 monoclonal antibody did not bind to lipopolysaccharides of the homologous strain, but cross-reacted with heterologous gram-negative rods in an enzyme-linked immunosorbent assay. These three monoclonal antibodies activated complement when incubated with homologous or heterologous strains, but were opsonic neither in the presence nor in the absence of complement. The other three monoclonal antibodies were directed against lipopolysaccharide of the homologous strain, but showed no cross-reactivity. The IgG3 and one IgM anti-J5 monoclonal antibodies activated complement and were opsonic only in the presence of complement. The IgM anti-O111 monoclonal antibody activated complement and was opsonic both in the presence and absence of complement. Thus, the outcome of the interaction between bacteria, antibodies, and complement is influenced primarily by whether antibodies are directed against lipopolysaccharides or against other cell wall components.

Animals↗
PubMed1986

Cross-reactivity of monoclonal antibodies against lipopolysaccharides of gram-negative bacteria.

Monoclonal antibodies were produced against Escherichia coli O111, Escherichia coli J5, and the rough (R) mutant of Salmonella typhimurium M206, and tested by enzyme-linked immunosorbent assay against lipopolysaccharides of several gram-negative strains. The monoclonal antibodies were also identified with an immunoblotting assay. Anti-Escherichia coli O111 monoclonal antibodies reacted only with homologous O antigens. Anti-J5 monoclonal antibodies cross-reacted with core lipopolysaccharide, especially with Rc lipopolysaccharide. IgM anti-J5 monoclonal antibodies showed more extensive cross-reactivity than IgG3 monoclonal antibodies. Anti-Re monoclonal antibodies cross-reacted weakly with all rough lipopolysaccharide tested. Thus, the varying specificity of these monoclonal antibodies seems to indicate that the core regions in the lipopolysaccharides of various gram-negative bacteria are not similar.

Animals↗
PubMed1986

Modulation of adherence of coagulase-negative staphylococci to Teflon catheters in vitro.

The mechanism of adherence of Staphylococcus epidermidis to commercially available catheters was studied in vitro in a quantitative assay employing 3H-labelled bacteria. It was found that adherence to Teflon catheters was significantly related to the degree of hydrophobicity of the strains. When hydrophobic groups were removed from Staphylococcus epidermidis by pepsin treatment, adhesion was almost completely abolished. Preincubation of catheters in human serum also caused a 80-90% reduction of adherence. Preincubation of Staphylococcus epidermidis in serum similarly decreased adhesion. This effect of serum was mainly due to albumin, while IgG and fibronectin were less effective. Culture of Staphylococcus epidermidis in subinhibitory concentrations (0.5 MIC) of cephalothin, clindamycin and vancomycin resulted in a 30-80% reduction in adhesion.

Anti-Bacterial Agents↗
PubMed1986

Modulation of phagocytic cell function.

Phagocytosis is an important factor in the defense of the host against all kinds of microorganisms. The process of phagocytosis of microorganisms by phagocytes can be separated into distinct but interrelated phases: adherence, chemotaxis, opsonization, attachment, ingestion, degranulation and killing. Phagocytosis is accompanied by an increase in oxygen metabolism in which H2O2 and activated oxygen species are generated. Modulation of phagocytic cell function can be brought about by a variety of substances. Microorganisms produce and contain components which influence the process of phagocytosis. Surrounding tissue cells and the phagocytes themselves produce biologically active molecules that modulate phagocytosis.

Arachidonic Acids↗
PubMed1986

Bactericidal, bacteriolytic and opsonic activity of human serum against Escherichia coli.

The effect of human serum on Escherichia coli was studied with serum-sensitive and serum-resistant strains. The bactericidal effect of human serum on serum-sensitive strains of E. coli depended on the activation of the classical complement pathway. The role of activation of the alternative pathway was less important. After incubation in sub-bactericidal concentrations of serum these strains were also easily phagocytosed by polymorphonuclear leukocytes (PMNL). Strains of E. coli of certain O-types required not only an intact classical pathway but also the presence of specific antibodies for effective killing by serum and effective phagocytosis by PMNL, despite rapid activation of complement and rapid deposition of C3 on the bacterial surface in the absence of antibody. Capsulate strains O1K1 and O78K80 resisted the bactericidal effect of serum even in the presence of specific antibodies; phagocytosis by PMNL only occurred after opsonisation with specific antibodies.

Antibodies, Bacterial↗
PubMed1986

Antibodies raised against rough mutants of Escherichia coli and Salmonella strains are opsonic only in the presence of complement.

The opsonic capacity of antisera raised in rabbits against rough (R) mutants and smooth (S) parent strains of Escherichia coli and Salmonella typhimurium were studied. All specific antibodies in the antisera belonged to the immunoglobulin G (IgG) class. Radioactively labeled bacteria were preincubated in various dilutions of antisera, in which complement was inactivated. Fresh normal rabbit serum, as a standard complement source, was used in some experiments. After preincubation, washed bacteria were added to normal human neutrophils. Opsonization of R mutants for 5 min in 5% fresh normal rabbit serum resulted in effective phagocytosis; S strains needed at least a 30-min opsonization time or 20 to 50% serum. After incubation for 5 min in diluted, homologous antisera, phagocytosis of S strains was optimal, but preincubation of R mutants in diluted, homologous antisera did not lead to amelioration of phagocytosis compared with that of bacteria preincubated in buffer only. However, when fresh normal serum was added to homologous antisera, uptake of R mutants occurred at a faster rate than that of bacteria opsonized in fresh serum alone. Using six clinical isolates of members of the family Enterobacteriaceae, we found that, with or without complement, antisera raised against E. coli J5 or S. typhimurium Re had, with the exception of one strain, no opsonic activity for these strains. Thus, the protective effect of R antisera in gram-negative bacteremia, as shown by several investigators, is unlikely to be mediated through enhanced opsonization of invading bacteria by IgG antibodies directed against these R mutants.

Animals↗
PubMed1986

Characterization of the alpha-MSH-like immunoreactivity in blood and cerebrospinal fluid of the rat.

We have investigated the nature of the alpha-melanocyte stimulating hormone-like immunoreactivity (alpha-MSH-LI) in blood and cerebrospinal fluid (CSF) of the rat. Blood and CSF from intact animals were subjected to high pressure liquid chromatography (HPLC) followed by a radioimmunoassay (RIA) specific for the C-terminal part of the alpha-MSH molecule. It appeared that in both body fluids the predominant alpha-MSH-LI co-migrated with synthetic alpha-MSH and not with its des-acetyl or di-acetyl analogues. We conclude that alpha-MSH is the predominant form of alpha-MSH-LI circulating in plasma and CSF of rats from our Wistar strain.

Animals↗
PubMed1986

[3H]9-desglycinamide,8-arginine vasopressin: metabolism and in-vivo fate.

Half-lives based on the disappearance of [3H]9-desglycinamide,8-arginine vasopressin ([3H]DGAVP) following in-vitro incubation in plasma were 1.7 h (dog), 5.8 h (rat) and greater than 12 h (man). For all three species, and particularly dogs, biotransformation of the peptide in plasma occurred predominantly through carboxypeptidase activities, leading to the accumulation of AVP-(1-7). Disappearance of [3H]DGAVP from rat blood after a single i.v. injection followed a biphasic decay with half-lives of 2.2 +/- 0.8 (S.D.) min (distribution phase) and 14.4 +/- 1.2 min (elimination phase). The central and peripheral volumes of distribution were high and of the same order of magnitude, being 0.21 and 0.25 litres/kg respectively. Blood clearance values ranged from 36 to 45 ml/min per kg. In addition to [3H]AVP-(1-7), [3H]tyrosine was also found to be a major radioactive metabolite in blood. Compared with i.v. dosing, the s.c. route of administration for [3H]DGAVP resulted in longer-lasting peptide levels in blood which persisted for up to 4-5 h after injection. Maximal concentrations were reached at 7.5 min, whereafter they declined bi-exponentially with terminal half-lives of 31.1 +/- 8.7 min. The mean bioavailability for DGAVP was almost 100%, demonstrating virtually complete absorption from the s.c. injection site.

Animals↗
PubMed1986

Cytotoxicity by human adherent cells: oxygen-dependent and -independent cytotoxic reactions by different cell populations.

Human adherent cells, obtained by EDTA reversible adherence to plastic, are potent effectors in cell-mediated cytotoxicity. Spontaneous cytotoxicity in a 2-hr assay against K562 target cells was shown to be largely mediated by contaminating natural killer (NK) cells. Treatment of adherent cells with NK-specific monoclonal antibody anti-Leu-11 plus complement abolished almost completely the spontaneous cytotoxicity. Spontaneous cytotoxicity by adherent cells was also reduced when the phorbol ester PMA was present in the assay. On the other hand, PMA induced a cytotoxic response in NK-cell depleted adherent cells after prolonged 18 hr incubation. The cell population responsible for this dichotomous effect of PMA on adherent cell-mediated cytotoxicity was shown to be monocytes, as revealed by monoclonal antibody treatment. Pure NK cell preparations were not affected by PMA in their cytolytic capacities. Reactive oxygen species are not involved in NK-cell mediated cytotoxicity, while PMA stimulated the monocytes to exert cytolysis and suppressed NK cells by the generation of these highly toxic oxygen products. Hydrogen peroxide especially seemed to be the mediator in this oxygen-dependent monocyte-mediated cytotoxicity and NK-cell suppression.

Catalase↗
PubMed1985

N alpha-Acetyl-gamma-endorphin is an endogenous non-opioid neuropeptide with biological activity.

N alpha-acetyl-gamma-endorphin (Ac gamma E) was identified in the rat neurointermediate pituitary, based on its immunological properties, comigration with synthetic Ac gamma E on HPLC and resistance to aminopeptidase-M degradation. The peptide appeared to be the main form of gamma-endorphin (gamma E) in this tissue and in brain areas remote from the hypothalamus (hippocampus, septum, amygdala). The anterior pituitary, the hypothalamus and the thalamus contained almost exclusively the non-acetylated form of gamma E. In contrast to gamma E, Ac gamma E was completely devoid of specific affinity for brain opiate binding sites. Yet, the peptide mimicked gamma E in that it potently attenuated passive avoidance behaviour in rats, when injected topically into the nucleus accumbens. It is concluded that Ac gamma E is an endogenous neuropeptide with non-opioid biological activity. N alpha-acetylation may not merely represent a mechanism for the inactivation of opioid activities of endorphins, but rather allow the organism to select specific sets of biological activities that reside in the endorphin structure.

Acetylation↗