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Biomedical subjects

J Verhoef

Publications and source records attributed to J Verhoef.

At least 505 records · Page 28Linked to original sources
PubMed1983

Synergy between the iron chelator deferoxamine and the antimicrobial agents gentamicin, chloramphenicol, cefalothin, cefotiam and cefsulodin.

Synergy between the iron chelator deferoxamine in the presence or absence of ascorbic acid and gentamicin, chloramphenicol, cephalothin, cefotiam or cefsulodin, used against Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, proteus mirabilis and species of Salmonella, Enterobacter, Pseudomonas and Providencia, was determined by measuring the effect of the drugs and combination of drugs on growth of the bacteria in an automated turbidimeter. The combination of drugs was considered to be synergistic when the growth inhibiting effect of the combination was greater than that of the combined action of each of the drugs separately. Deferoxamine plus ascorbic acid together with either gentamicin or cefsulodin showed synergy in 10 out of 10, and 5 out of 6 cultures respectively, whereas deferoxamine plus ascorbic acid with chloramphenicol, cephalothin or cefotiam was synergistic in 6 out of 14, 5 out of 11, and 3 out of 6 cultures. This synergistic effect was much lower when microorganisms were incubated with deferoxamine combined with the various antibiotics but without ascorbic acid. Ascorbic acid alone had no synergistic effect. When deferoxamine was saturated with iron, its antibacterial effect was completely abolished.

Alcaligenes↗
PubMed1983

Characterization of N alpha-acetyl-alpha-endorphin from rat neurointermediate lobe and its distribution in pituitary and brain.

N alpha-Acetyl-alpha-endorphin was characterized from rat neurointermediate lobe. The distribution of the acetylated and the non-acetylated form of alpha-endorphin in dissected areas of pituitary and brain appeared to be uneven. alpha-Endorphin appeared to be the main peptide in the anterior pituitary, whereas in the neurointermediate lobe N alpha-acetyl-alpha-endorphin accounted for most of the alpha-endorphin immunoreactivity. In the brain, the highest concentration of alpha-endorphin immunoreactivity was found in the hypothalamus. In hypothalamus and thalamus alpha-endorphin predominated, whereas in amygdala, hippocampus and septum N alpha-acetyl-alpha-endorphin represented most of the alpha-endorphin-immunoreactivity. In view of the non-opioid properties of acetylated endorphins, it is suggested that acetylation represents a mechanism allowing the organism to specifically select the non-opioid behavioral activities enclosed in the endorphin sequence.

Animals↗
PubMed1983

Activation of purified human plasma prekallikrein triggered by cell wall fractions of Escherichia coli and Staphylococcus aureus.

Whether Escherichia coli and Staphylococcus aureus cell wall fractions can trigger the activation of prekallikrein was investigated in a mixture of purified human factor XII, prekallikrein, and high-relative-molecular-weight (Mr) kininogen. After exposure for 30 min to bacterial preparations (0.02-5 mg/ml) at 0 C, lallikrein amidolytic activity was expressed as a percentage of the optimal activation of prekallikrein induced by dextran sulfate. Lipopolysaccharide (LPS) fractions of five E coli strains and lipid A of E coli O111B4 induced 50%-90% optimal activity. However, the polysaccharide fraction induced less than 5% activity. Peptidoglycan and teichoic acid of S aureus induced 70%-100% optimal activity at 5 mg/ml, but protein A did not generate activity. No activation of prekallikrein occurred in the absence of factor XII. Thus, LPS and lipid A of E coli and peptidoglycan and teichoic acid of S aureus can generate kallikrein amidolytic activity in a mixture of purified factor XII, prekallikrein, and high-Mr kininogen.

Cell Wall↗
PubMed1983

Clindamycin enhances opsonization of Staphylococcus aureus.

Staphylococcus aureus 502A was grown in the presence of one-third of the minimal inhibitory concentration of clindamycin. Phagocytosis of the antibiotic-treated bacteria by human polymorphonuclear leukocytes was significantly enhanced, compared with that of the untreated control (P less than 0.001). Study of opsonization kinetics by a chemiluminescence assay demonstrated that clindamycin-treated staphylococci were opsonized more rapidly than control bacteria and that the serum concentration required for sufficient opsonization was lower. Complement was consumed much faster, and the opsonic fragment C3b was fixed more rapidly to the bacterial surface when the staphylococci were preincubated with clindamycin. Electron micrographs showed an alteration of the staphylococcal cell wall after clindamycin treatment.

Blood Bactericidal Activity↗
PubMed1983

Escherichia coli lipopolysaccharides diminish and enhance cell function of human polymorphonuclear leukocytes.

The effects of the lipopolysaccharide (LPS) of Escherichia coli J5 and 0111B4 on the function of human polymorphonuclear leukocytes (PMN) were tested. E. coli J5 is a UDP-galactose-4-epimerase-deficient mutant of E. coli 0111B4, and its LPS, therefore, contains mainly lipid A, as it lacks the polysaccharide side chains. PMN which had been incubated with J5 LPS showed decreased phagocytic, chemotactic, and metabolic activities as compared with control PMN. In contrast, incubation of PMN with 0111B4 LPS had no effect or even an enhancing effect on PMN function. When lipid A and the polysaccharide fraction were isolated from 0111B4 LPS, it was shown that lipid A had the same deleterious effect on PMN function as did J5 LPS and that the LPS fraction had no effect. When PMN were incubated with J5 LPS or lipid A, it could be shown that these structures were able to induce PMN to generate superoxide and chemiluminescence. 0111B4 LPS and the polysaccharide component were able to generate a metabolic burst by the PMN to a lesser extent. The induced defects in PMN function by J5 LPS could be prevented when polymyxin B or an oxygen-radical scavenger was present. We hypothesize that the lipid A portion of LPS is toxic for PMN due to the induction of toxic oxygen species by the PMN. These toxic oxygen species destroy the phagocytic, chemotactic, and metabolic activities of the PMN.

Chemotaxis, Leukocyte↗
PubMed1983

Biology and clinical significance of peptidoglycan antibody response in staphylococcal infections.

Peptidoglycan, the basic structure of the staphylococcal cell wall, is a matrix of glycan strands that are cross-linked through short peptide side chains. Many of the biological activities of staphylococcal cells can be ascribed to the peptidoglycan moiety of their cell walls. Staphylococcal peptidoglycan can be shown to be immunogenic in laboratory animals; both humoral and cellular immune responses have been noted. Sensitive techniques, such as radio- or enzyme-immunoassay, have recently shown that virtually all normal human donors have detectable peptidoglycan IgG antibodies in their serum. Peptidoglycan IgG can be transplacentally transferred. The titers of peptidoglycan antibody vary widely among healthy donors. Increased production of peptidoglycan antibodies is found in most patients with complicated S. aureus septicaemia and also in many with uncomplicated bacteremia. Nonbacteremic S. aureus infections usually do not stimulate peptidoglycan antibody production. Compared to other S. aureus products such as teichoic acid, nuclease, and alpha-toxin, peptidoglycan may be the most sensitive antigen for detecting antibody responses during staphylococcal infections. Peptidoglycan antibodies may neutralize some of the toxic effects of the staphylococcal cell wall and promote phagocytosis of the organisms. However, increased peptidoglycan antibody titers with immuno-complex disease have also been associated with longstanding infections due to S. epidermidis, Streptococci and with rheumatoid arthritis. Thus, peptidoglycan antibodies may cross-react among Gram-positive bacterial species and have detrimental effects as well.

Antibodies, Bacterial↗
PubMed1983

Staphylococcus epidermidis endocarditis and Staphylococcus epidermidis infection in an intensive care unit.

Staphylococcus epidermidis are the most common agents of prosthetic valve endocarditis (PVE). S. epidermidis isolated from the blood stream of patients with PVE are almost invariably multiple resistant to antibiotics. Antibiotic treatment alone gives unsatisfactory results and carries a mortality rate of 70-80%. That is why early surgical treatment is recommended. S. epidermidis is a less common cause of endocarditis in non-surgical patients, accounting for approximately 5% of the cases, which are mostly patients with pre-existent valvular heart disease. Generally, isolates from the latter patients are sensitive to most antibiotics, and the mortality rate is considerably lower. Recently coagulase-negative staphylococci have emerged as causative agents of septicaemia in patients hospitalized in intensive care units. Especially premature infants of very low-birth weight (less than 1500 g) receiving parenteral nutrition appear to carry a high risk of acquiring this kind of septicaemia. Although the staphylococci isolated from the blood of these patients are the same as in patients with PVE, generally multiple resistant to antibiotics, prognosis is far better than in cases of PVE. In our study carried out in a neonatal intensive care unit, two risk factors for coagulase-negative staphylococcal septicaemia were identified. First, nearly 20% of parenteral nutrition fluids used in the unit were found to be contaminated with coagulase-negative staphylococci, and a significant association was established between septicaemia and the infusion of contaminated fluids. Moreover, opsonization of staphylococci in infant serum proved to be severely deficient. Since host defence to staphylococci is dependent on optimal opsonization of these microorganisms, this defence may be severely compromised in the premature neonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Recognition of Staphylococcus aureus by human phagocytes. Signals and disguises of the bacterial surface.

Phagocytic cells provide the host its major defense against invasive Staphylococcus aureus, and the staphylococcal surface, by its influence on phagocyte recognition, is a primary determinant of the function of these cells. The peptidoglycan component of the cell wall plays a key role in both opsonic and chemotactic recognition, mediated by IgG, C3b, and C5a, respectively. While cell wall protein A inhibits opsonic recognition by polymorphonuclear leukocytes, it promotes an opsonin-independent mechanism of phagocytosis by human macrophages which possess cytophilic IgG. By masking cell wall-associated opsonic molecules, capsular polysaccharides inhibit recognition, a phenomenon that is overcome by specific anti-capsular antibodies. It is proposed that impaired phagocyte recognition is a basic element in the pathogenesis of staphylococcal endocarditis, and progress in the prevention and treatment of this infection may depend on understanding the basis for this host defense defect.

Animals↗
PubMed1983

The effect of staphylococcal peptidoglycan on polymorphonuclear leukocytes in vitro and in vivo.

The ability of Staphylococcus aureus to resist phagocytosis by polymorphonuclear leukocytes (PMN) is thought to be an important virulence factor for this microorganism. We have studied the effect of peptidoglycan (PG) on PMN function in vitro, and on the induction of leukopenia in vivo. Phagocytosis and chemotaxis by human PMN were both inhibited in vitro by prior incubation with as little as 2.5 micrograms PG/ml. Control PMN phagocytized 85% of added bacteria, while PMN treated with PG for 30 minutes phagocytized only 45% of the bacteria. Also, PG-treated PMN did not migrate towards an attractant. Suppression of PMN function by PG could be abolished when PG was incubated with antiserum raised in rabbits against PG. PMN incubated with PG generated a burst in oxygen metabolism as measured by the emission of chemiluminescence. When PG (500 micrograms) was given to rats or guinea pigs, the animal developed an early leukopenia which paralleled a drop in blood pressure and in thrombocyte levels, and in the concentration of hemolytic complement. Leukopenia was less in animals treated with cobravenom; an agent known to deplete complement. Antihistaminics had no effect on the induction of leukopenia by PG. We conclude that PG may be at least partly responsible for leukopenia sometimes observed in patients with life-threatening staphylococcal infections, and this leukopenia might be due to a direct or indirect toxic effect of PG on the PMN.

Adult↗
PubMed1983

Inherited deficiency of the third component of complement associated with recurrent pyogenic infections, circulating immune complexes, and vasculitis in a Dutch family.

A family is described in which 3/11 children showed a homozygous deficiency of C3, and both parents and six other children had subnormal levels of C3. The three children with selective C3 deficiency suffered repeatedly from bacterial infections, whereas the parents and the other siblings were clinically healthy. During infectious episodes the patients showed a maculopapular skin rash, and at such times immune complexes were present in the serum. Biopsy specimens of the skin lesions showed the picture of leukocytoclastic vasculitis.

Adolescent↗
PubMed1983

Inhibition of human natural killer activity by lysosomotropic agents.

We have examined the effect of three lysosomotropic amines on human NK cell activity. Dansylcadaverine (DCA), diphenylamine (DPA), and lidocaine (LID) inhibited NK activity of nylon wool-purified and large granular lymphocyte (LGL)-enriched cell preparations. Cadaverine (CAD), an analog of DCA that does not affect lysosomal function, had no effect on NK activity. Binding of the K562 target cells to effector cells, as assessed in a single cell assay, was not inhibited by DCA, DPA, or LID. Cytotoxicity was inhibited by DCA and DPA only when these drugs were added within 5 min after the initiation of NK assays. In contrast, LID inhibited NK activity even when added 60 min after the addition of effector cells to target cells. All three amines that inhibited NK activity also reduced the intracellular concentration of the lysosomal enzyme beta-glucuronidase without affecting the activity of the cytoplasmic enzyme lactate dehydrogenase. Kinetic analysis revealed that LID inhibited both the maximum velocity (Vmax) of the cytotoxicity reaction as well as the affinity constant (Km); whereas DCA and DPA only inhibited Vmax.

Adult↗
PubMed1982

Listeria monocytogenes meningitis and decreased phagocytosis associated with iron overload.

A patient with Listeria monocytogenes meningitis was found to have idiopathic haemochromatosis and monocytes with reduced phagocytic capacity. The phagocytic function recovered completely after a series of therapeutic phlebotomies. In-vitro iron had a deleterious effect on the phagocytic capacity of monocytes and granulocytes. These findings show that iron overload in the host can increase susceptibility to L monocytogenes infection not only by increasing the virulence of the organism but also by reducing the phagocytic capacity of the monocytes.

Bloodletting↗
PubMed1982

Regional distribution of alpha- and gamma-type endorphins in rat brain.

The regional distribution of Met-enkephalin, beta-endorphin and alpha- and gamma-type endorphins in rat brain was investigated. To that end, brains were dissected into anatomically defined areas. Acetic acid tissue extracts were fractionated using an HPLC system suitable for separation of endorphins and peptide concentrations were subsequently measured by specific radioimmunoassay systems. The distribution of Met-enkephalin and beta-endorphin through the brain was fairly uneven and in accordance with results obtained by others. The peptides alpha-endorphin, gamma-endorphin, des-Tyr-alpha-endorphin (DT alpha E) and des-Tyr-gamma-endorphin (DT gamma E) were detectable in almost all brain areas. Their distribution, however, appeared to be uneven. Hypothalamus and septum showed the highest levels of alpha- and gamma-type endorphins. These regions also contained high amounts of beta-endorphin, underscoring a precursor function of this peptide in the formation of alpha- and gamma-type fragments. In general, levels of alpha-endorphin were higher than those of des-Try-alpha-endorphin, whereas the opposite was found for gamma- and des-Tyr-gamma-endorphin.

Animals↗
PubMed1982

Serum-induced lysis of Pseudomonas aeruginosa.

The sensitivity of 12 Pseudomonas aeruginosa strains (5 mucoid and 7 non-mucoid strains) to serum and the interaction of these strains with the complement system was studied. Five strains (4 mucoid and 1 non-mucoid strains) were lysed in 20% normal serum as measured by the release of radiolabelled material from 3H-adenine labelled bacteria. Three of these strains were also lysed in MgEGTA chelated serum. All strains activated complement via the classical pathway, and six strains were able to activate the alternative complement pathway as well. Slime production did not interfere with bacteriolysis and complement consumption.

Bacteriolysis↗