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Biomedical subjects

J Verhoef

Publications and source records attributed to J Verhoef.

At least 523 records · Page 29Linked to original sources
PubMed1982

Opsonization and phagocytosis of mucoid and non-mucoid Pseudomonas aeruginosa strains.

The interaction between Pseudomonas aeruginosa strains (6 non-mucoid and 4 mucoid strains), serum factors and phagocytic cells was investigated. Strains were incubated in different concentrations of normal serum, chelated serum (with only the alternative complement pathway intact), IgG, Cls, C2 and C3 deficient serum and immune serum. After incubation complement consumption, C3 fixation and phagocytosis by polymorphonuclear leukocytes (PMN) were measured. In contrast to normal serum, immune serum raised against a mucoid and a non-mucoid strain exhibited heat-stable opsonic activity. All ten Pseudomonas aeruginosa strains were able to activate complement in 20% normal serum, leading to deposition of the activated form of the third complement component on the bacterial cell wall and to subsequent recognition and phagocytosis. One mucoid and four non-mucoid strains activated the alternative complement pathway and were effectively opsonized in chelated or in Cls, C2 or IgG deficient serum. Although mucoid strains were less able to activate complement via the alternative route, no differences were observed in opsonic requirements and phagocytosis between mucoid and non-mucoid strains.

Complement System Proteins↗
PubMed1982

Effect of influenza virus on phagocytic cells.

Many viral infections predispose to bacterial superinfection, and it has been suggested that the increased susceptibility to bacterial infections is at least in part due to the effect of virus on the phagocytic cell function. Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2] ) treated leukocytes with 3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 10(7) EID50 units of influenza virus, PMNs ingested only 35% of the bacteria, whereas control leukocytes ingested over 80%. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.

Blood Bactericidal Activity↗
PubMed1982

Role of peptidoglycan from Staphylococcus aureus in leukopenia, thrombocytopenia, and complement activation associated with bacteremia.

The role of the major cell wall components of Staphylococcus aureus in the leukopenia, thrombocytopenia, and complement activation associated with S. aureus bacteremia was studied in a guinea pig model. Formalin-killed S. aureus strains HSmR, 52A5, Cowan I, and Cowan EMS and purified peptidoglycan were used. Normal animals given peptidoglycan developed early (5-min) leukopenia, thrombocytopenia, and depletion of C3-C9 hemolytic activity similar to values in animals given killed S. aureus organisms and C4-deficient animals challenged with peptidoglycan. Cobra venom factor-treated animals challenged with peptidoglycan did not develop early leukopenia and thrombocytopenia, but all animal groups persistently had late (greater than 1-hr) leukopenia and thrombocytopenia. This observation suggests that peptidoglycan may play a major role in the early leukopenia and thrombocytopenia associated with S. aureus bacteremia in the guinea pig and that these effects can be mediated by activation of the alternative complement pathway alone. Peptidoglycan also causes a late leukopenia and thrombocytopenia which may occur independently of complement activation.

Animals↗
PubMed1982

H-Pro-[3H]Leu-Gly-NH2: plasma profile and brain uptake following subcutaneous injection in the rat.

Following subcutaneous injection of the tripeptide H-Pro-[3H]Leu-Gly-NH2 ([3H]PLG) in rats, the profile of intact peptide and its radioactively labeled metabolites was examined both in plasma and in brain tissue. [3H]PLG and metabolites were determined in trichloroacetic acid extracts by reverse-phase paired-ion HPLC. Maximal plasma levels of unmetabolized PLG were reached 6-8 min after administration, after which they decreased with an elimination half-life of 20 min. The uptake of [3H]PLG in the brain ranged from 0.0013% to 0.0017% of the administered dose per g tissue at 6-30 min following subcutaneous injection. After comparing these results with our previous findings with intravenous injection of [3H]PLG, it seemed likely that the subcutaneous route of administration might be more effective in eliciting CNS effects of PLG than the intravenous route of administration. The metabolite profiles in plasma and brain point to an initial cleavage of PLG at the NH2-terminal side and a very rapid degradation of the peptide intermediate H-Leu-Gly-NH2.

Animals↗
PubMed1982

H-Pro-[3H]Leu-Gly-NH2: uptake and metabolism in rat brain.

The uptake and metabolism of H-Pro-[3H]Leu-Gly-NH2 ([3H]PLG) in rat brain was investigated by reverse-phase paired-ion high pressure liquid chromatography. Following in vitro incubation of [3H]PLG with rat brain subcellular preparations, the microsomal-cytosol fraction was about twice as active in degrading PLG as the crude mitochondrial-synaptosomal fraction. For both enzyme preparations the pH optimum was found at pH 7-7.5. The major labeled metabolite was [3H]leucine, whereas 3H]labeled Leu-Gly-NH2 as the only labeled peptide intermediate was found in trace amounts. After intravenous injection of [3H]PLG the uptake of unmetabolized peptide in the brain appeared to be very low: 0.008% and 0.001% of the administered dose/g tissue at 2 and 5 min after injection respectively, while at longer survival times intact peptide was below the detection limit. Compared with the intravenous route of administration, intracerebroventricular injection of [3H]PLG yielded much higher brain concentrations of unmetabolized PLG. Following both routes of administration, the metabolite profile was in agreement with that obtained after in vitro incubation. However, the in vivo experiments also showed considerable incorporation of [3H]leucine liberated from [3H]PLG into proteins. Both the in vitro and in vivo results indicate that the initial cleavage of PLG in rat brain occurs at the NH2-terminus and that the dipeptide intermediate H-Leu-Gly-NH2 is subsequently hydrolyzed to its constituent amino acids very rapidly.

Animals↗
PubMed1982

Prostatitis due to penicillinase-producing Neisseria gonorrhoeae. Case reports.

Complicated infections caused by penicillinase-producing Neisseria gonorrhoeae (PPNG) are uncommon. Of two patients with prostatitis due to PPNG, one was cured by cefoxitin followed by co-trimoxazole, the other by co-trimoxazole alone. The potential of co-trimoxazole in the treatment of PPNG-prostatitis looks promising.

Adult↗
PubMed1982

Human alveolar macrophage cytophilic immunoglobulin G-mediated phagocytosis of protein A-positive staphylococci.

Human alveolar macrophages (AM) have recently been reported to ingest and kill a strain of Staphylococcus (502A) in the absence of opsonins. To further investigate the mechanism of non-opsonic recognition, we studied phagocytosis of 23 clinical and laboratory strains of S. aureus and Staphylococcus epidermidis by AM, and by blood polymorphonuclear leukocytes (PMN) and monocytes (MN). In the absence of opsonins, AM phagocytized 18 protein A-positive but not 5 protein A-negative strains of staphylococci, and the efficiency of phagocytosis directly correlated with the amount of protein A present in the bacterial cell wall (r = 0.86, P less than 0.001). Furthermore, AM rosetted around protein A-coated Sepharose beads, but not around beads without protein A. In contrast, PMN did not phagocytize nonopsonized staphylococci, and did not rosette around either type of Sepharose. MN phagocytized protein A-positive staphylococci, but much less efficiently than AM, and showed some rosetting around protein A-coated Sepharose. The nature of the AM receptor for protein A-positive staphylococci was studied. The surface of AM was positively stained with fluorescein-conjugated antibody to human IgG, but not with IgA- or IgM-specific conjugates. No such surface-immunoglobulins were detected on PMN, and MN were only weakly positive for surface IgG. Pretreatment of AM with F(ab')2 fragments specific for human IgG (anti-Fc) inhibited subsequent phagocytosis of protein A-positive staphylococci. There was no evidence that the AM surface IgG was aggregated or immunecomplexed. From these studies we conclude that human AM possess cytophilic IgG antibodies, which can function as receptors for phagocytosis of protein A-positive staphylococci.

Animals↗
PubMed1982

Neutrophil function, serum opsonic activity, and delayed hypersensitivity in surgical patients.

The phagocytic function (e.g., phagocytosis, chemiluminescence, and chemotaxis) of polymorphonuclear leukocytes (PMNs), delayed hypersensitivity, and serum opsonic capacity were studied in 29 patients who underwent major surgical procedures, primarily abdominal surgery. The phagocytic capacity and chemiluminescence were normal in all patients as compared with healthy donors, and no difference in phagocytosis was found before or after operation. However, PMNs of 14 patients (48%) showed diminished chemotactic activity after surgery, but the influence of surgery on chemotaxis could not be demonstrated. About 30% of the patients had depressed delayed hypersensitivity after operation, as measured by skin testing using three recall antigens. The mean induration of the skin tests was 6.9 +/- 3.4 mm before operation and 3.6 +/- 2.9 mm thereafter (P = 0.006). The opsonic capacity of patient sera was measured as uptake by normal donor PMNs of staphylococci opsonized in patient serum. Eleven of 19 preoperative serum samples had an opsonic capacity comparable to that of normal control sera; the opsonic capacity of postoperative serum samples of the same patients was significantly decreased as compared with preoperative values. In seven patients the opsonic capacity of postoperative serum samples correlated with decreased levels of IgG in the sera but not with complement activity.

Adult↗
PubMed1981

Antibodies to cell wall peptidoglycan of Staphylococcus aureus in patients with serious staphylococcal infections.

An enzyme-linked immunoassay was used to detect antibodies to the cell wall peptidoglycan of Staphylococcus aureus in human sera. All 170 sera from donors and patients with staphylococcal and nonstaphylococcal infections contained IgG antibodies to peptidoglycan; antibody levels varied with age, and transplacental transfer occurred. IgM antibodies to peptidoglycan were not found in donors and were present in only one patient with serious staphylococcal infection. Significantly elevated levels of IgG antibodies to peptidoglycan were observed in 20 (80%) of 25 patients with deep tissue infection with S. aureus but in only two (9%) of 22 patients with superficial staphylococcal infection. An increase in levels of antibodies to peptidoglycan generally coincided with an increase in level of IgG antibodies to teichoic acid. No cross-reactivity between peptidoglycan and teichoic acid was observed. Thus, staphylococcal peptidoglycan is immunogenic in humans, and testing for IgG antibodies to peptidoglycan may be useful in the diagnosis and follow-up of serious staphylococcal infections.

Antibodies, Bacterial↗
PubMed1981

Escherichia coli antibodies in opsonisation and protection against infection.

The opsonic and protective capacities of rabbit antisera against Escherichia coli O, K and core-glycolipid cell-wall antigens were compared with specific antibody titres as measured by agglutination and enzyme-linked immunosorbent assay. Anti-O antisera were opsonic and protective against two noncapsulate strains. Only anti-K antisera were opsonic and protective against a K-antigen-containing strain. In a mouse model anti-core-glycolipid antiserum was not protective against challenge even by a strain bearing only core glycolipid.

Animals↗
PubMed1981

Initiation of the respiratory burst of human neutrophils by influenza virus.

The role of the oxygen-dependent microbicidal systems of polymorphonuclear neutrophils in virus inactivation is not known. We found that isolated neutrophils responded to incubation with purified influenza virus A particles by consumption of oxygen, generation of chemiluminescence, and production of superoxide; these reactions occurred in the absence of serum. Resting leukocyte oxygen consumption doubled in the presence of virus; the average rate of consumption 2 to 12 min after virus was added was 1.54 nmol/10(7) cells per min. Live virus also stimulated superoxide production in a dose-dependent manner at a rate up to 4.54 nmol/10(7) cells per min. Luminol-amplified chemiluminescence was a rapid dose-dependent reaction which peaked 2 to 4 min after live or ultraviolet light-inactivated virus was added. No light was emitted when heat-inactivated virus particles were used, suggesting that heat-labile factors on the virus envelope may be involved in oxidative stimulation. Virus-stimulated neutrophils from a patient with chronic granulomatous disease emitted no light. The evidence that virus initiated the respiratory burst of neutrophils provided a potential mechanism for virus destruction, either by direct intracellular inactivation or by neutrophil-mediated cellular cytotoxicity of virus-infected target cells.

Antiviral Agents↗
PubMed1981

Human fibronectin binding to staphylococcal surface protein and its relative inefficiency in promoting phagocytosis by human polymorphonuclear leukocytes, monocytes, and alveolar macrophages.

The interaction between human fibronectin and 17 strains of staphylococci was studied in an attempt to elucidate the staphylococcal cell wall component(s) involved in fibronectin binding and to determine the influence of fibronectin upon phagocytosis by three types of phagocytic cells. Purified, radiolabeled fibronectin bound to a similar degree to six laboratory strains and three fresh clinical isolates of Staphylococcus aureus; similar binding of fibronectin was found with S. aureus strains deficient in cell wall teichoic acid or clumping factor and coagulase, as well as with three strains of S. epidermidis. There was minimal binding of fibronectin to encapsulated S. aureus and to Escherichia coli. Fibronectin bound to intact cells and to a crude cell wall preparation of S. aureus H, but not to purified cell walls or peptidoglycan. Trypsinization of staphylococci prevented subsequent fibronectin binding, but binding did not correlate well with the protein A content in S. aureus cell walls. At physiological concentrations, fibronectin binding to staphylococci did not promote phagocytosis of bacteria by human polymorphonuclear leukocytes, monocytes, or alveolar macrophages. Also, depletion of fibronectin from normal human serum did not result in a measurable loss of opsonic activity for staphylococci. It is concluded that fibronectin binding to staphylococci involves a surface protein shared among strains of S. aureus and S. epidermidis, and that in comparison to C3b and IgG, fibronectin plays a relatively minor role as an opsonin for staphylococci.

Bacterial Proteins↗
PubMed1981

Protein A effect on alternative pathway complement activation and opsonization of Staphylococcus aureus.

Twelve Staphylococcus aureus strains with known amounts of protein A were compared with regard to alternative pathway complement activation and opsonization in human serum. "Protein A-poor" strains (less than or equal to 0.16 ng/10(6) bacteria) were, on the average, 3. 4-fold more efficient in alternative pathway complement activation than "protein A-rich" strains (greater than or equal to 0.625 ng/10(6) bacteria) (P less than 0.001). Protein A-poor strains were significantly better phagocytized by human polymorphonuclear leukocytes after opsonization in magnesium-ethylene glycol-bis (beta-amino-ethyl ether)-N, N-tetraacetic acid-chelated serum than were the protein A-rich strains (P less than 0.001). No significant differences between protein A-poor and -rich strains were found in complement activation and opsonization in normal serum. Cell wall-bound protein A appeared to hinder alternative pathway complement activation by S. aureus, which resulted in decreased opsonization of these bacteria in the absence of an intact classical pathway. These studies suggest that protein A may cover alternative pathway complement-activating sites within the peptidoglycan matrix of the staphylococcal cell wall.

Complement Activation↗
PubMed1981

Prevention of infection by trimethoprim-sulfamethoxazole plus amphotericin B in patients with acute nonlymphocytic leukaemia.

Fifty-two patients with nonlymphocytic leukaemia were studied during remission induction treatment in a randomized trial to ascertain the effect of prophylactic oral trimethoprim-sulfamethoxazole on infection and fever rate. A decrease in the total number of acquired infections was found (16 infections in the group given trimethoprim-sulfamethoxazole versus 31 in the control group, p less than 0.01). The number of patients without any infection in the trimethoprim-sulfamethoxazole group was 13 compared to only three in the control group (p less than 0.01). Patients in the trimethoprim-sulfamethoxazole group needed parenteral antibiotics during 33% of the days they were granulocytopenic compared to 61% of these days for patients in the control group. However, six of nine bacteriologically documented infections in the trimethoprim-sulfamethoxazole group were caused by resistant microorganisms compared to two out of 20 in the control group.

Acute Disease↗