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Biomedical subjects

H van Dijk

Publications and source records attributed to H van Dijk.

At least 55 records · Page 3Linked to original sources

Phenotypic characterization of epidemic versus sporadic strains of methicillin-resistant Staphylococcus aureus.

Forty strains of methicillin-resistant Staphylococcus aureus (MRSA) were divided on the basis of their epidemiologic behavior into two subgroups, sporadic MRSA (SMRSA) and epidemic MRSA (EMRSA) strains. The strains were examined for binding of 125I-labelled fibronectin, vitronectin, collagen, Fc fragments of immunoglobulin G, and fibrinogen. A significant difference between EMRSA and SMRSA strains was found for binding of 125I-labelled fibrinogen and for Fc fragments of immunoglobulin G, (P < 0.05). No significant difference in the binding of 125I-labelled fibronectin and collagen was found between EMRSA and SMRSA strains. The binding of 125I-labelled vitronectin to MRSA strains was found to be aspecific. Capsular serotypes of the strains were determined with monoclonal antibodies against capsular types 5 and 8. Strains could be divided into the following four groups: types 5, 8, and 5/8 and nontypeable. More nontypeable strains were found in the EMRSA group (66.6%). Significantly more EMRSA strains (79%) than SMRSA strains (44%) produced alpha-toxin (P < 0.025). Logistic regression analysis using a combination of the parameters 125I-labelled immunoglobulin G binding, capsular type, and alpha-toxin production predicted the epidemic character with a sensitivity of 83% and a specificity of 75%.

Bacterial Toxins↗

Experimental evidence for Moraxella-induced penicillin neutralization in pneumococcal pneumonia.

Resistance of microorganisms to antimicrobial agents is an increasing problem in the treatment of infectious diseases. In mixed infections, an interesting development can arise when one organism protects another from being killed by an antibiotic. Unfortunately, in the case of respiratory tract infections, experimental evidence of this development is poor. In this study, mice intranasally infected with a lethal number of pneumococci and treated with a curative dose of penicillin or amoxicillin died from pneumococcal pneumonia when they were coinoculated with beta-lactamase-producing Moraxella catarrhalis. beta-lactamase-negative M. catarrhalis did not show a similar indirect pathogenic effect. Treatment with a combination of amoxicillin and the beta-lactamase inhibitor clavulanic acid was not affected by beta-lactamase-producing M. catarrhalis. These findings help explain antibiotic failure in respiratory tract infections, even though the causative microorganism is sensitive to the antibiotic in vitro.

Amoxicillin↗

Protective effects of orally administered, Klebsiella-containing bacterial lysates in mice.

The efficacy, as oral vaccines, of hepta- and mono-valent, Klebsiella-containing bacterial lysates and a number of control preparations was tested in mice. The preparations were administered during two periods of four days each, interrupted by an interval of 3 days. Fourteen days after the first dose, the animals were challenged either intraperitoneally (i.p.; peritonitis/sepsis model) or intranasally (i.n.; pneumonia model). Animals treated with low doses of Klebsiella lysate, in the form of either a 7-valent lysate or a Klebsiella monolysate, showed enhanced survival in both the peritonitis/sepsis and the pneumonia models. Hexa- and tetra-valent preparations without Klebsiella were not protective in the models tested. Furthermore, it was found that the protection is accompanied by priming for Klebsiella-specific IgG responsiveness (probably at the T cell level) and by significant IgA anti-Klebsiella serum antibody levels in about one third of the animals. The oral efficacy of Klebsiella-containing lysates suggests the presence of an adjacent component that directs Klebsiella antigen(s) to follow a selective intestinal pathway which renders them immunogenic. The identity of this component is under investigation.

Administration, Oral↗

Differences in complement activation between complement-resistant and complement-sensitive Moraxella (Branhamella) catarrhalis strains occur at the level of membrane attack complex formation.

The mechanism of resistance to human complement-mediated killing in Moraxella catarrhalis was studied by comparing different complement-sensitive and complement-resistant M. catarrhalis strains in a functional bystander hemolysis assay and an enzyme-linked immunosorbent assay (ELISA) for soluble terminal complement complexes. Complement-resistant stains appeared to activate complement to the same extent as, or even slightly better than, complement-sensitive strains. This indicates that complement-resistant strains do not inhibit classical or alternative pathway activation but interfere with complement at the level of membrane attack complex formation. A clear difference in dose-response curves for resistant and sensitive strains was observed both in the bystander hemolysis assay and in the ELISA. Complement-resistant strains showed optimum curves, whereas complement-sensitive strains gave almost linear curves. We conclude that resistant strains bind and/or inactivate one of the terminal complement components or intermediates involved in membrane attack complex formation. Trypsin, known to abolish complement resistance, changed the optimum dose-response curve of a resistant strain to a linear one, which strongly suggests that complement resistance is mediated by an M. catarrhalis-associated protein. This protein acts directly or through the binding of a terminal complement inhibitor present in serum.

Bacterial Proteins↗

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↗

Bacterium-induced autoimmune reactivity.

Evidence is growing that autoimmune reactivity results from a combination of endogenous (e.g. MHC type) and environmental factors. Our experimental study focuses on the induction of autoimmune reactivity by microbial factors. Splenic formation and serum levels of anti-erythrocyte antibodies and circulating immune complexes were taken as parameters. It was found that experimental infection of mice with Escherichia coli and Salmonella typhimurium was accompanied by clear signs of autoimmune reactivity, smooth bacteria being almost ten times as potent as rough mutant strains. An attempt was made to correlate the data obtained with live bacteria to their corresponding endotoxins. It was concluded that the induction of more prominent autoimmune reactivity by smooth bacteria must be ascribed to a longer survival time in vivo. Our data support the view that bacterium-derived factors are involved in the etiology (and possibly also the course) of autoimmune diseases.

Animals↗

Rapid isolation of human complement component C9 to verify the specificity of a haemolytic C9 microassay.

A sensitive, haemolytic microassay of human complement component C9 was developed. The assay is based on the principle of reactive (C5b6-initiated) haemolysis and uses commercially available C9-depleted serum as reagent for C9. The specificity of the assay was verified by rapid, activity-guided isolation of the haemolytic component from human serum using high-performance liquid chromatography (HPLC) on a system for fast protein liquid chromatography. This isolation yielded a single component with characteristics of C9. The results suggest that rapid, activity-guided isolation as a new application of HPLC can be a useful tool to demonstrate the specificity of a functional assay.

Adult↗

C1-inhibitor prevents PEG fractionation-induced, EDTA-resistant activation of mouse complement.

Fractionation of mouse serum by precipitation with a critical amount of polyethylene glycol 6000 (PEG; 11% w/v) results in a classical and alternative pathway-independent activation of the terminal complement route. The activation can take place after the separation of an activating principle together with the terminal route components from a natural regulator. The isolation and identification of the regulatory component preventing this activation in serum, is subject of this paper. The regulator was purified by fractionated PEG-precipitation (15-25%), followed by heparin-Sepharose affinity, Mono Q anion-exchange, and Superose 12 gel filtration chromatography. The regulator appeared to be a single-chain protein with a Mr of 96 k. A protein with similar activity purified from human serum had a Mr of 104 k and was functionally and antigenically indistinguishable from C1-INH. The mouse 96 k protein inhibited C1-esterase activity indicating that this protein is indeed C1-INH. Mouse C1-INH regulates the PEG fractionation-induced bypass activation of complement, but does not interfere with the assembly or the lytic activity of membrane attack complexes. alpha 2-Macroglobulin appeared also to be capable of inhibiting the PEG-precipitation-induced activation process, but with lower efficiency.

Animals↗

Anti-inflammatory activity of gallic acid.

Gallic acid was found to possess antiinflammatory activity towards zymosan-induced acute food pad swelling in mice. In vitro studies on the mode of action of gallic acid revealed that this compound interferes with the functioning of polymorphonuclear leukocytes (PMNs). Scavenging of superoxide anions, inhibition of myeloperoxidase release and activity as well as a possible interference with the assembly of active NADPH-oxidase may account for the inhibition of inflammatory process by gallic acid. Structure-activity relationship analysis showed that the o-dihydroxy group of gallic acid is important for the inhibitory activity in vitro.

Animals↗

C5 does not play a major role in the immune response of mice to SRBC in vivo.

The role of complement component C5 in the immune response of mice to sheep red blood cells (SRBC) was investigated. Congenic C5-sufficient and C5-deficient B10. D2 mice and genetically C5-deficient DBA/2 mice, as such or supplemented with C5-sufficient serum, were used as experimental animals. C5-substitution of the C5-deficient mice resulted in measurable C5 levels for days. The functional half-life of C5 in C5-deficient DBA/2 mice was about 21 h. No significant differences between the IgM-responses of C5-bearing and naive C5-deficient animals were observed. This suggests that C5 does not play a major role in the primary humoral immune response of mice in vivo, although C5 seems to do so in in vitro experiments, even with the same antigen. Antigen-induced C5-production by C5-deficient mice as one of the explanations of the in vitro/in vivo discrepancy could not be confirmed experimentally.

Animals↗

Induction of auto-antibody formation in C3H/HeJ mice by cobra venom factor.

Recently, we demonstrated that lipopolysaccharide (LPS)-hyporesponsive C3H/HeJ mice show a very high background number of splenic antibody-forming cells with specificity for bromelain-treated isologous erythrocytes. This background level was not or only slightly enhanced by LPS injection. In this paper it is reported that the existing response of C3H/HeJ mice is about doubled by treatment of the animals with cobra venom factor (CVF). This increase is very similar to the LPS-induced potentiation of the auto-antibody response of C3H/Tif and other LPS-responder mice. The absence of auto-antibodies in the sera of CVF-treated C3H/HeJ mice, however, points at a different mechanism of B cell activation. The mediation of the CVF-induced stimulation of the B cells of C3H/HeJ mice by covalent C3-glycoprotein complexes and the need for an additional stimulus is discussed.

Animals↗

Induction of active immunological hypo/non-responsiveness to C5 in adult C5-deficient DBA/2 mice.

Injection of C5-sufficient BALB/c serum rendered DBA/2 mice (C5-deficient) immunologically hypo- or non-responsive to C5. This was indicated by C5-elimination studies in the C5-deficient mice showing similar half-lives for C5 upon single and repeated BALB/c serum injection. Concrete evidence for C5 non-responsiveness came from experiments showing that C5-injected DBA/2 mice were unable to mount an anti-C5 antibody response after active immunization with C5-sufficient serum in Freund's complete adjuvant. C5 hypo/non-responsiveness could be induced in DBA/2 mice via the intravenous as well as the intraperitoneal route, provided the C5-sufficient serum was administered in the very narrow dose range of 10-100 microliters (approximately 0.3-3 micrograms of C5). Upon i.v. C5 injection, C5 non-responsiveness was nearly complete on Day 4 and lasted about 3 weeks. Hyporesponsiveness was still present 6 weeks after serum injection. C3-/C5-depleting cobra venom factor reversed tolerization for C5, at least when applied within 48 hr after i.v. C5 injection. Similarity between the acquired C5 hypo/non-responsiveness of DBA/2 mice and the established C5 tolerance of BALB/c mice was suggested by adoptive cell transfer experiments: spleen cells from naive DBA/2 mice stimulated B cells of C5-sufficient nude mice to produce C5-neutralizing antibodies. In contrast, splenocytes from C5-tolerized DBA/2 mice, like those of BALB/c mice, did not decrease haemolytic C5 levels in C5-sufficient nude mice.

Animals↗

Effects of low molecular constituents from Aloe vera gel on oxidative metabolism and cytotoxic and bactericidal activities of human neutrophils.

In traditional South-East Asian medicine the therapeutic value of the parenchymous leaf-gel of Aloe vera for inflammatory-based diseases is well-reputed. The aim of this study is to investigate at which level gel-constituents exert their activity. We show here that low -Mr constituents of an aqueous gel-extract inhibit the release of reactive oxygen species (ROS) by PMA-stimulated human PMN. The compounds inhibit the ROS-dependent extracellular effects of PMN such as lysis of red blood cells. The capacity of the PMN to phagocytose and kill micro-organisms at the intracellular level is not affected. The inhibitory activity of the low-Mr compounds is most pronounced in the PMA-induced ROS production, but is significantly antagonized by the Ca-ionophore A23187. It is shown that the inhibitory effect of the low-Mr compounds is the indirect result of the diminished availability of intracellular free Ca-ions.

Aloe↗

Endotoxin-induced auto-immunity in mice. III. Comparison of different endotoxin preparations.

Six different endotoxin preparations derived from Escherichia coli and Salmonella typhimurium subspecies were compared as to their potencies to provoke auto-immune phenomena in mice. The numbers of spleen cells forming antibodies to bromelain-treated isologous erythrocytes or anti-DNA antibodies, the serum levels of these auto-antibodies, and the circulating immune complex titres were determined. As far as comparison on a weight base was concerned, S. typhimurium Re-mutant lipopolysaccharide appeared to be the most active preparation in inducing auto-antibody formation. Upon comparison of amounts with equal activity in the limulus amoebocyte lysate assay, however, S. typhimurium lipid A turned out to be the most potent. The contribution of O-type specific polysaccharides, phosphate groups, and the lipid A moiety to the potencies of the endotoxin preparations is discussed.

Animals↗

Trial and error in producing ankylosing-spondylitis-selective antisera according to Andrew Geczy.

Geczy found that rabbit sera raised against Klebsiella strain K43 cross-reacted with the cells from HLA-B27 positive patients with ankylosing spondylitis (AS). Other laboratories failed to reproduce these results. After a series of unsuccessful attempts, however, we managed to prepare one selective antiserum, using E. coli, isolated from a Dutch Bechterew patient, in offspring of rabbits Geczy sent us. Ever since we obtained irreproducible results only. This paper reports about the many attempts we have made to produce a discriminating antiserum for use in a combined vital stain and dye-exclusion assay.

Animals↗

Immunodulatory compounds from Picrorhiza kurroa: isolation and characterization of two anti-complementary polymeric fractions from an aqueous root extract.

Two aqueous root extracts of Picrorhiza kurroa, one prepared by extraction at 4 degrees C and the other by refluxing, were purified using the guidance of modulation of classical (CP) and alternative (AP) pathway complement activity. By means of methanol extraction and gel filtration chromatography, two polymeric fractions were isolated from the cold water extract. A methanol-soluble polymeric fraction (CS1) was highly active in inhibiting CP complement activity exclusively, whereas a methanol-insoluble polymeric fraction (CI1) exhibited an inhibitory effect on both CP and AP complement activity. Preliminary chemical analysis of the anti-complementary fractions revealed the presence of structures of carbohydrate and of peptide nature in CS1 and CI1. The modulation of CP complement activity by CS1 was studied in more detail. Its inhibitory effect was proven to be based on complement consumption rather than on chelation of Ca2+ and/or Mg2+ or on stabilization of the target cells in the complement-assay. The purification of the aqueous extract prepared by refluxing, resulted in the isolation of a polymeric fraction with the same qualities as CS1. However, a fraction with properties similar to CI1 could not be isolated from this extract.

Adjuvants, Immunologic↗