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Biomedical subjects

J Verhoef

Publications and source records attributed to J Verhoef.

At least 289 records · Page 16Linked to original sources
PubMed1993

Chemiluminescence of human polymorphonuclear leucocytes after stimulation with whole cells and cell-wall components of Staphylococcus epidermidis.

The purpose of this study was to define cell-wall components of Staphylococcus epidermidis responsible for activation of human polymorphonuclear leucocytes (PMNL). Metabolic activation of PMNL was determined by chemiluminescence (CL). Purified peptidoglycan (PG) induced a concentration-dependent metabolic burst in PMNL. The minimal concentration needed for CL induction was 1 microgram/ml. Comparison between different S. epidermidis strains showed variation in the capacity to induce CL in PMNL. Purified PG induced a higher CL response in PMNL than its intact parent strain; this effect was found in all S. epidermidis strains. Lipoteichoic acid (LTA), PG stem peptide and muramyldipeptide (MDP) did not induce CL; teichoic acid induced a CL response only at very high concentrations. No differences in CL inducing capacity were found between PG, crude cell walls, and purified cell walls of S. epidermidis. Sonication of PG strongly diminished CL-inducing capacity. PG treatment with mutanolysin immediately resulted in decreased CL-inducing capacity. Treatment of PG with S. aureus lytic enzyme (SALE) 10 micrograms/ml for up to 15 min enhanced the CL response to PMNL; a similar increase in CL was induced by PG treated with SALE at 1 microgram/ml for up to 120 min. Beyond these times, a continuous decrease in PG-induced CL was observed. In conclusion, PG was found to be the major cell-wall component of S. epidermidis involved in CL induction. Moreover, a minimal fragment size or a specific tertiary structure of PG, or both, is required for metabolic activation of PMNL.

Adult↗
PubMed1993

Peptidoglycan and teichoic acid from Staphylococcus epidermidis stimulate human monocytes to release tumour necrosis factor-alpha, interleukin-1 beta and interleukin-6.

Cytokines play a major role in the pathophysiology of septic shock. In this study, human peripheral blood monocytes were stimulated with peptidoglycan and teichoic acid, purified from a strain of Staphylococcus epidermidis. Polymyxin B (PM-B) was added to avoid the effects of possible contamination with endotoxin. Tumour necrosis factor-alpha (TNF), interleukin-1 beta (IL-1), and interleukin-6 (IL-6) in the supernates were measured by enzyme-linked immunosorbent assays. Peptidoglycan and teichoic acid induced TNF, IL-1, and IL-6 in a concentration-dependent manner. Teichoic acid was a weaker inducer than peptidoglycan, especially for IL-1. Lipopolysaccharide from an E. coli strain was used as a control, being 100-1000 times more potent than peptidoglycan and teichoic acid.

Enzyme-Linked Immunosorbent Assay↗
PubMed1993

Changes in adherence of respiratory pathogens to HEp-2 cells induced by subinhibitory concentrations of sparfloxacin, ciprofloxacin, and trimethoprim.

Preincubation with subinhibitory concentrations of sparfloxacin, ciprofloxacin, and trimethoprim decreased the adherence of the respiratory pathogens Klebsiella pneumoniae, Haemophilus influenzae, and Moraxella (Branhamella) catarrhalis to human larynx carcinoma HEp-2 cells. Subinhibitory concentrations of sparfloxacin did not change the adherence of Pseudomonas aeruginosa or Streptococcus pneumoniae 15.62, but adhesion of S. pneumoniae 15.42 was significantly enhanced by subinhibitory antimicrobial concentrations.

Anti-Infective Agents↗
PubMed1993

Detection of Listeria monocytogenes in cheese with the magnetic immuno-polymerase chain reaction assay.

A new detection system, the magnetic immuno-polymerase chain reaction (PCR) assay (MIPA) has been developed to detect Listeria monocytogenes in food. This method separates Listeria cells from PCR-inhibitory factors present in enrichment broths containing food samples by using magnetic beads coated with specific monoclonal antibodies (MAbs). The separated bacteria were lysed, and the supernatant containing the bacterial DNA was subjected to the PCR. Detection of L. monocytogenes in three naturally contaminated cheese samples with two different MAbs and PCR primers specific for the gene encoding the delayed-hypersensitivity factor showed that with MAb 55 all three samples were positive whereas with MAb A two samples were positive. A further improvement of the method was obtained by using a PCR step based on the listeriolysin O gene. A MIPA employing MAb 55 and the listeriolysin O gene primer set detected L. monocytogenes after 24 h of culture in Listeria Enrichment Broth samples from Port Salut artificially contaminated with 40 CFU/25 g. We could detect 1 CFU of L. monocytogenes per g of cheese after a second enrichment for 24 h in Fraser broth. The analysis time including both enrichments is approximately 55 h.

Antibodies, Monoclonal↗
PubMed1993

Rapid detection of salmonellae in poultry with the magnetic immuno-polymerase chain reaction assay.

Rapid detection of salmonellae in chicken meat was accomplished by using the magnetic immuno-polymerase chain reaction assay (MIPA). A direct polymerase chain reaction assay performed with chicken meat spiked with Salmonella typhimurium resulted in poor sensitivity (approximately 10(7) CFU/g of meat). The use of immunoseparation with a Salmonella serogroup B-specific monoclonal antibody improved the sensitivity, but enrichment was required for the detection of low levels of contamination. Enrichment for 6 h in either buffered peptone water, lactose broth containing tergitol-7, or selenite-cystine broth resulted in the detection of an initial inoculum of 100 CFU per g of meat. Enrichment of the salmonellae present on 25 g of spiked chicken meat for 24 h in either buffered peptone water or selenite-cystine broth before detection by the MIPA yielded a detection limit of approximately 0.1 CFU/g of meat. A detection limit of approximately 1 CFU/g of meat was obtained when the spiked meat was stored at -20 degrees C before enrichment for 24 h and analysis with the MIPA. Although the MIPA was developed for S. typhimurium, a MIPA in which a panel of six monoclonal antibodies specific for Salmonella serogroups A through E was used detected the presence of 0.1 CFU of Salmonella enteritidis per g of chicken meat. These data indicate that the method is applicable to other commonly isolated serotypes.

Animals↗
PubMed1993

Monoclonal antibodies that react with live Listeria spp.

Seven monoclonal antibodies (MAbs) against Listeria spp. that were reactive with live Listeria spp. were developed. Two of these MAbs (55-8 and 55-37) were members of the immunoglobulin M class, and all other MAbs were members of the immunoglobulin G class. MAb 55-23 reacted with 148 of 157 strains tested. MAb 34-51 reacted with serotype 1/2a, 1/2b, and 1/2c strains and exhibited a scattered reaction pattern with strains belonging to other serotypes. MAb 55-44 reacted with all of the strains belonging to serotype 4b tested. MAb 55-4 reacted with all of the serotype 1/2a isolates tested, although reactivity with other isolates also was observed. The other MAbs exhibited scattered reaction patterns. No correlation of reactivity pattern with serotype was found. Marked differences were observed between the reactivities of MAbs as determined by a magnetic immunoluminescence assay and a whole-cell enzyme-linked immunosorbent assay. Only MAb 55-23 exhibited minor reactivity with three Streptococcus spp. isolates, while no reactivity was observed with six Bacillus spp. strains, one Escherichia coli strain, and one Citrobacter sp. strain. In Western blots (immunoblots) MAbs 55-23, 55-44, and 34-9 exhibited reactivity; all other MAbs were negative in this assay.

Animals↗
PubMed1993

Meningococcal lipopolysaccharide (LPS)-derived oligosaccharide-protein conjugates evoke outer membrane protein- but not LPS-specific bactericidal antibodies in mice: influence of adjuvants.

Meningococcal lipopolysaccharide (LPS)-derived oligosaccharides (OS) were coupled to tetanus toxoid (TT) and purified P1.7,16 outer membrane proteins (OMP). The immunogenicities of the conjugates with and without the addition of the adjuvant Quil A or the nonionic block polymer L121 were studied in mice. Immunotype L2 and L3,7,9 OS-TT conjugates induced immunoglobulin G (IgG) responses that were strongly augmented by Quil A and L121. These adjuvants not only enhanced the amount of IgG evoked but also shifted the IgG subclass distribution from mainly IgG1 toward the complement-activating subclasses IgG2a and IgG2b. The antibodies induced were directed against the OS part of meningococcal LPS. They were not bactericidal for group B meningococci. Both the L3,7,9 OS-P1.7,16 OMP conjugate and purified P1.7,16 OMP evoked a strong IgG response against the P1.7,16 OMP but not against the L3,7,9 LPS. These anti-OMP IgG responses were comparable to the IgG OMP-specific responses induced by the H44/76 or HIII-5 outer membrane vesicles but still did not lyse group B meningococcal strains. The IgG response evoked with OS-OMP or purified OMP consisted mainly of the IgG1 subclass, whereas the H44/76 or HIII-5 outer membrane vesicles induced high amounts of bactericidal IgG2a and IgG2b antibodies next to the IgG1 antibodies. The addition of the adjuvant Quil A or L121 to OS-OMP or OMP resulted in the induction of high levels of bactericidal anti-P1.7,16-specific OMP antibodies, as reflected by the presence of substantial amounts of IgG2a and IgG2b antibodies. These results indicate that (i) mouse anti-LPS antibodies evoked by LPS-derived OS-protein conjugates are not bactericidal for group B meningococci, (ii) extensive purification of P1.7,16 OMP can lead to the loss of the intrinsic adjuvant properties of outer membrane vesicle preparations, and (iii) the addition of suitable adjuvants restores the ability of these purified P1.7,16 OMP to induce bactericidal antibodies.

Adjuvants, Immunologic↗
PubMed1993

Induction of release of tumor necrosis factor from human monocytes by staphylococci and staphylococcal peptidoglycans.

The role of cytokines in gram-positive infections is still relatively poorly defined. The purpose of this study was to establish whether or not intact staphylococci and purified peptidoglycans and peptidoglycan components derived from staphylococci are capable of stimulating the release of tumor necrosis factor (TNF) by human monocytes. We show here that intact staphylococci and purified peptidoglycans, isolated from three Staphylococcus epidermidis and three S. aureus strains, were indeed able to induce secretion of TNF by human monocytes in a concentration-dependent fashion. TNF release was detected by both enzyme immunoassay and the L929 fibroblast bioassay. In the enzyme immunoassay, a minimal concentration of peptidoglycan of 1 micrograms/ml was required to detect TNF release by monocytes, whereas in the bioassay a peptidoglycan concentration of 10 micrograms/ml was needed to detect a similar amount of TNF release. Peptidoglycan components such as the stem peptide, tetra- and pentaglycine, and muramyl dipeptide were unable to induce TNF release from human monocytes.

Cell Wall↗
PubMed1993

Tumor necrosis factor alpha (TNF-alpha) production in mice immunized with Escherichia coli: correlation with mortality after lethal challenge and production of a native inhibitor of TNF-alpha activity.

The kinetics of tumor necrosis factor alpha (TNF-alpha) production, the correlation between cytokine levels and mortality rates after lethal challenge, and the production of a native inhibitor of TNF-alpha activity was investigated in mice immunized with formalin-killed Escherichia coli. Groups of mice were injected for 8 weeks with either untreated bacteria or bacteria treated with 0.5 MIC of aztreonam and subsequently challenged with 100 50% lethal doses of viable E. coli. Mice receiving saline only (controls) died within 24 h. The mortality of mice immunized with aztreonam-treated E. coli was significantly lower than that of mice immunized with untreated E. coli. There were no measurable levels of TNF-alpha in sera obtained from control mice during the entire period of immunization. TNF-alpha levels ranging from 90 to 306 U/ml were measured 90 min after each vaccination in sera obtained from mice immunized with untreated E. coli. Sera from mice immunized with antibiotic-treated E. coli showed lower TNF-alpha levels, ranging from 40 to 128 U/ml. TNF-alpha levels measured 90 min after lethal challenge correlated with the mortality rate observed in each group (r = 0.95). The cytotoxic activity of recombinant murine TNF-alpha was inhibited by the sera from immunized mice but not by the sera from controls. The inhibition was drastically reduced by preincubation of the sera with staphylococcal protein A. In immunoblot experiments, class G immunoglobulins reacting with recombinant murine TNF-alpha were observed in the sera of immunized mice. These data confirm the correlation existing between TNF-alpha levels and mortality and suggest that native inhibitors may play a role in the regulation of the biological function of the cytokine.

Animals↗
PubMed1993

Escherichia coli in bacteremia: O-acetylated K1 strains appear to be more virulent than non-O-acetylated K1 strains.

A total of 174 blood isolates of Escherichia coli, collected during a 5-year period at the University Hospital Utrecht, were serotyped with rabbit sera against 171 O antigens and 73 capsule (K) antigens. The four most prevalent O-antigen serotypes were O6 (n = 22), O18 (n = 19), O1 (n = 19), and O2 (n = 15). Thirty-one strains were not typeable with any of the O-antigen-typing sera. Of the 148 strains that were subjected to K-antigen serotyping, 34 strains lacked a K antigen and 41 were not typeable with the K-antigen-specific antisera used in the study. K1 was by far the most frequently found K-antigen serotype; this was followed by K2, K53, K5, K13, K7, K(A)28, and K15. Strains possessing a K1 antigen were further classified as either O-acetyl-positive (n = 12) or O-acetyl-negative (n = 21) strains. Retrospective analysis of patients infected with different E. coli isolates--nonencapsulated (n = 23), O-acetylated K1 (n = 12), and non-O-acetylated K1 (n = 21)--revealed clinical differences. More patients suffered from sepsis (94% versus 74%), and a higher rate of mortality was found in the group infected with K1 isolates (18 versus 9%) than in the group infected with nonencapsulated isolates. More patients with severe sepsis (25 versus 10%) and a higher mortality (33 versus 10%) were found in the group infected with O-acetylated K1 isolates than in the group infected with non-O-acetylated isolated. Also, the hospitalization of these patients was prolonged. Thus, O-acetylated E. coli K1 strains seem to be more virulent than non-O-acetylated K1 strains.

Acetylation↗
PubMed1993

Comparison of typing methods for Clostridium difficile isolates.

A simple discriminative typing method for Clostridium difficile has been developed. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of whole-cell proteins and restriction enzyme analysis are relatively simple techniques but are difficult to evaluate, especially the restriction enzyme analysis. Immunoblotting and restriction fragment length polymorphism typing facilitate simple discrimination of patterns.

Bacterial Typing Techniques↗
PubMed1993

Comparison of three days' therapy with cefcanel or amoxicillin for the treatment of acute uncomplicated urinary tract infection.

The clinical and bacteriologic efficacy of 3 days of cefcanel daloxate therapy, compared with 3 days of amoxicillin for the treatment of acute uncomplicated urinary tract infection was compared in a prospective randomized double-blind multicentre study. 400 subjects were randomized to receive cefcanel daloxate and 199 to receive amoxicillin. 166 (77%) of 215 evaluable cefcanel daloxate subjects and 72 (77%) of 94 evaluable amoxicillin subjects evidenced bacteriologic elimination at short-term follow-up, while in 149 (69%) and 67 (71%), respectively, clinical symptoms disappeared. At long-term follow-up, 150 (70%) cefcanel daloxate and 65 (69%) amoxicillin subjects evidenced bacteriological elimination, while in 150 (70%) and 61 (65%), clinical symptoms disappeared. There were no significant differences in outcome between the 2 therapeutic regimens. Adverse events were similar in the 2 groups. In additional analyses, antimicrobial efficacy diminished significantly with increasing age, pretherapy in vitro susceptibility was significantly associated with bacteriological failure at the short-term visit, and subjects with low quantitative counts pretherapy had clinical outcomes similar to those with quantitative counts > or = 10(5) cfu/ml at the short-term outcome. These data suggest that cefcanel daloxate and amoxicillin are comparable as regards efficacy and adverse effects for 3-day therapy of acute uncomplicated urinary tract infection. The observed cure rates, however, are lower than those reported for other agents such as trimethoprim/sulfamethoxazole or quinolones for short course therapy.

Acute Disease↗
PubMed1993

Serum-independent binding of lipopolysaccharide to human monocytes is trypsin sensitive and does not involve CD14.

The nature of the binding sites for lipopolysaccharide (LPS) on human monocytes was investigated using fluorescein isothiocyanate (FITC)-labelled LPS from Salmonella minnesota R595 (ReLPS). In the absence of serum, ReLPS bound to monocytes and this interaction was trypsin sensitive. A concentration of 0.1 mg/ml resulted in a 90% loss of LPS binding, while low concentrations increased this binding. Trypsin-treated monocytes recovered FITC-ReLPS binding after 20 hr culture, which was abrogated in the presence of cycloheximide and actinomycin D. This showed that de novo protein and mRNA synthesis were essential. A number of different proteins have been implicated in cellular binding of LPS to monocytes. In this paper we show that CD14 is not involved in direct binding of FITC-ReLPS to monocytes, since anti-CD14 monoclonal antibody (mAb) (3C10) and removal of most of cell-surface CD14 by phosphatidylinositol-specific phospholipase C did not prevent FITC-ReLPS binding. Furthermore, LPS also bound to CD14-deficient cells from a patient with paroxysmal nocturnal haemoglobinuria (PNH). FITC-ReLPS binding was not mediated by the CD11/CD18 complex since mAb to the alpha and beta chains of the CD11/CD18 complex did not alter the binding of FITC-ReLPS to cells. These observations indicate that ReLPS may interact with monocyte membrane protein(s) in the absence of serum. This binding site(s) for LPS might be different from those previously described by others.

Antigens, CD↗
PubMed1993

Anti-idiotypic immunization provides protection against lethal endotoxaemia in BALB/c mice.

Against lipid A (the conserved moiety of lipopolysaccharides from Gram-negative bacteria) neutralizing IgM monoclonal antibodies (mAb) 8-2 and 26-20 anti-idiotypic (Ab2) mAb were produced: Ab2 mAb KM-04 (IgG1) against mAb 8-2, and Ab2 mAb PW-1 (IgG2a) and PW-2 (IgG1) against mAb 26-20. The binding of Ab2 mAb KM-04 to 8-2 (Ab1) was strongly inhibited by a lipopolysaccharide (LPS) extract from either Salmonella minnesota R595 (Re LPS) or Escherichia coli J5 (Rc LPS), whereas the binding of Ab2 mAb PW-1 and PW-2 to 26-20 (Ab1) was only marginally inhibited by both Re LPS and Rc LPS. The results indicated that Ab2 mAb KM-04 recognizes a lipid A-binding site related idiotope on mAb 8-2 and therefore KM-04 might bear the internal image of a neutralization determining epitope of lipid A. Consequently Ab2 KM-04 might induce antibodies to lipid A. Indeed anti-idiotypic immunization of syngeneic BALB/c mice with Ab2 mAb KM-04 resulted in development of lipid A-binding anti-anti-idiotypic (Ab3) antibodies in serum. Similar immunizations with Ab2 mAb PW-1 and PW-2 were unsuccessful. However, induction of lipid A-binding Ab3 by mAb KM-04 proved to be genetically restricted to BALB/c mice. DBA/2 mice, Swiss mice and rabbits did not develop lipid A-binding antibodies upon immunization with mAb KM-04. In protection experiments, it was shown that BALB/c mice vaccinated with mAb KM-04 showed significantly enhanced survival from challenge with either rough (Re) LPS from Salmonella minnesota or smooth LPS from E. coli 0111:B4 when compared to BALB/c mice immunized with a non-relevant Ab2 mAb. The results suggest that mAb KM-04 constitutes a non-internal image vaccine to the lethal effect of lipid A in BALB/c mice. Furthermore an Ab3 mAb was prepared against Ab2 mAb KM-04 that showed reactivity with Re LPS. This Ab3 mAb, designated LE-21 (IgG2a) protected mice against an otherwise lethal challenge of Re LPS.

Animals↗
PubMed1993

In vivo exposure to the currently available peritoneal dialysis fluids decreases the function of peritoneal macrophages in CAPD.

Previous in vitro studies have revealed that the currently available peritoneal dialysis fluids (PDF) inhibit several functions of phagocytic cells. To investigate the clinical relevance of those in vitro findings, we compared the in vivo effect of PDF pH on peritoneal macrophage (PMO) function in chronic peritoneal dialysis patients. In a randomized crossover setting, each of eight patients used exclusively PDF at pH five (D5) or pH seven (D7) on day one. The next day the patients who used D5 were switched to D7 and vice versa. Likewise the effect of glucose-mediated hypertonicity was studied in eight other patients, using PDF with 1.36% glucose (D136) or 3.86% glucose (D386). PMO were isolated from the effluents and studied for their phagocytic and killing capacity, and their ability to mount a respiratory burst (chemiluminescence response). PMO obtained after the intraperitoneal instillation of D7 were significantly better able to phagocytize both S. epidermidis (65 +/- 9 vs 37 +/- 8% uptake, p < 0.005) and E. coli (43 +/- 8 vs 25 +/- 4% uptake, p < 0.005). In addition, PMO harvested from D7 effluents revealed a significantly higher killing capacity than PMO derived from D5 effluents for S. epidermidis (60 +/- 5 vs 38 +/- 6%, p < 0.005) as well as for E. coli (51 +/- 10 vs 25 +/- 9%, p < 0.025). Moreover, PMO derived from D7 effluents mounted a significantly higher respiratory burst as compared to PMO in vivo exposed to D5 for the same time.(ABSTRACT TRUNCATED AT 250 WORDS)

Dialysis Solutions↗
PubMed1992

[Detection of diarrhea-causing Escherichia coli using DNA-probes].

To assess the role of enterovirulent Escherichia coli at home and abroad, faeces samples of patients with diarrhoea and of healthy controls in Tunisia, Seville (southern Spain) and the Netherlands were investigated. Enterovirulent E. coli were identified by hybridization with five different non-radioactively labelled DNA probes specific for enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC) and verocytotoxin producing E. coli (VTEC). ETEC was the main causative agent of travellers' diarrhoea in Tunisia. The isolation of ETEC in the Netherlands was shown to be related to travel in endemic areas. EPEC probe positive strains were isolated in children and in adults, but were not in all cases associated with intestinal disease. During this study no VTEC were detected. From an immunocompromised kidney transplantation patient with sepsis and diarrhoea ETEC were isolated from blood.

Adolescent↗
PubMed1992

Binding of surfactant protein A (SP-A) to herpes simplex virus type 1-infected cells is mediated by the carbohydrate moiety of SP-A.

Pulmonary surfactant protein A (SP-A) has been shown to act as an opsonin in the phagocytosis of viruses by alveolar macrophages. To determine whether SP-A binds to viral proteins and which part of the SP-A molecule is involved in this interaction, binding studies were undertaken. SP-A was labeled with fluorescein isothiocyanate, and its binding to herpes simplex virus type 1-infected HEp-2 cells, as a model for virus-infected cells in general, was studied using flow cytometry. The binding of SP-A to virus-infected cells was saturable, reversible, and both time- and concentration-dependent, reaching a maximal level after 30 min at an SP-A concentration of 10 micrograms/ml. An approximately 4-fold increase in binding of SP-A to infected cells over control cells was observed. Yeast mannan, a mannose homopolysaccharide, did not influence the binding. However, heparin inhibited binding of SP-A in a concentration-dependent manner. In addition, heparin could also dissociate cell-bound SP-A, indicating that polyanionic oligosaccharides are involved in the binding of SP-A to virus-infected cells. Deglycosylated SP-A, obtained by digestion with N-glycosidase F, did not bind to infected cells. Heparin or deglycosylation of SP-A had no effect on the stimulation of alveolar macrophages by SP-A. It is concluded that the carbohydrate moiety of SP-A is involved in the recognition of viruses by SP-A and may play a role in the antiviral defenses of the lung.

Animals↗