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PubMed2000

Concurrent measurement of antigen- and antibody-dependent oxidative burst and phagocytosis in monocytes and neutrophils.

The current study aims to review flow cytometric (FCM) parameters for the quantification of phagocytosis. A limitation of existing methods is their difficulty with accurate quantification of the phagocytic index, i.e., number of beads per phagocyte, in individual cell lines in mixed cell suspensions. We have quantified phagocytosis and the oxidative burst simultaneously using fluorescent beads coated with meningococcal outer membrane vesicles (OMV beads) by the conversion of dihydrorhodamine 123 (DHR-123) to rhodamine 123 (R-123). Both these processes depend on specific serum opsonins. After the incubation, staining with a fluorescent anti-CD14 monoclonal antibody succeeded in discriminating phagocytosing monocytes from neutrophils. The spectral overlaps between OMV beads, R-123, and anti-CD14 could be completely compensated. Percentage of phagocytosis and the phagocytic index were similar in monocytes and neutrophils, but the oxidative burst behaved differently. Two monocyte subpopulations were observed. Both subpopulations spontaneously converted some DHR-123 into R-123, whereas the reaction was triggered by phagocytosis in neutrophils. The total oxidative response increased with increasing phagocytic index in both cell types, but the oxidative burst in monocytes was about twice that of neutrophils. The oxidative ratio (mean R-123 fluorescence value divided by the phagocytic index) declined with time in monocytes, but increased in neutrophils. Our results demonstrate the need for careful attention to technical details. This single-laser, three-color FCM method facilitates the comparative research of phagocytosis and the oxidative burst in monocytes and neutrophils and provides a basis for a number of applications in hematology, infectious medicine, and immunology.

Antibodies, Monoclonal↗
PubMed1996

A possible mechanism for host-specific pathogenesis of Salmonella serovars.

We have identified the complement receptors on human and murine macrophages involved in the recognition of Salmonella serovars, and investigated their relevance to the intracellular survival. S. typhi was capable of surviving within human monocyte-derived macrophages, whereas S. typhimurium was not. Conversely, S. typhimurium, but not S. typhi, resisted intracellular killing by murine macrophages, demonstrating that the intracellular survival of Salmonella serovars is host-dependent. In the presence of serum opsonin, human monocyte-derived macrophages recognized S. typhi and S. typhimurium via complement receptor type 1 (CR1) and type 3 (CR3), respectively. In contrast, murine macrophages recognized S. typhi and S. typhimurium via CR3 and CR1, respectively. These findings demonstrate that the intracellular fate of Salmonella serovars following phagocytosis may depend on the type of complement receptors involved in their recognition, in that CR1-mediated recognition is closely correlated to subsequent intracellular survival. The Tn5 insertion mutant of S. typhimurium which lacks the ability to interact with CR1 was sensitive to intracellular killing by murine macrophages in vitro, and was much less virulent to mice in vivo, confirming the relevance of CR1-mediated bacterial recognition to the pathogenicity of S. typhimurium for mice. These results suggest that selective recognition of Salmonella serovars through CR1 may lead to their subsequent intracellular survival, and is responsible for the host-specific pathogenesis of Salmonella serovars.

Animals↗
PubMed1983

Partial myeloperoxidase deficiency in preleukemia.

In seven subjects with partial and apparently acquired form of myeloperoxidase (MPO) deficiency, some functional properties of neutrophils (PMNs) were studied. Five patients suffered from preleukemia, one from diabetes mellitus and one from carcinoma of the breast with bone marrow metastases. Intracellular bactericidal activity, oxygen consumption and superoxide radical production were within normal limits. In three patients with preleukemia, the serum opsonic activity was markedly reduced (less than m-3SD) in an autologous system, but normal in the presence of pooled normal serum. Decreased opsonic activity was also found when these patient's sera were assayed in the presence of normal PMNs. Since the levels of IgG and C3 were comparable in the patients' sera and the pooled serum, a deficiency of another unknown opsonin or the presence of an opsonization inhibitor has to be postulated. The partial MPO defect apparently doesn't decrease the intracellular killing of Staphylococcus aureus by PMNs. The known susceptibility to bacterial infections in preleukemia may be explained by the reduction of serum opsonization conducing to a secondary decrease of the ingestion and killing of bacteria by the PMNs.

Blood Bactericidal Activity↗
PubMed1978

Nitroblue tetrazolium-dye reduction by rat peritoneal macrophages during the uptake of Diplococcus pneumoniae, type VI.

The relationship between the rate of particle ingestion and the rate of Nitroblue Tetrazolium (NBT)-dye reduction by macrophages was studied after incubation of peritoneal exudate macrophages with heat-killed type VI pneumococci. The adherence to a polyethylene surface of the macrophages during the uptake of the pneumococci was determined as well. In some experiments pneumococci opsonized with heat-stable opsonins were used as material to be ingested. The NBT-dye reduction and the surface adherence of the macrophages was enhanced when ingesting normal heat-killed pneumococci. During the uptake of opsonized, heat-killed pneumococci the macrophages showed an unaltered NBT-dye reduction and less adherence to a polyethylene surface as compared with macrophages incubated with normal heat-killed pneumococci. This implies that using opsonized pneumococci the quantitative NBT-dye reduction assay is not reliable as a parameter for macrophage phagocytosis, because the uptake was in fact enhanced. The surface adherence of the macrophages did not reflect the enhanced ingestion of opsonized bacteria either.

Animals↗
PubMed1979

[Humoral defence against infection (author's transl)].

The importance of endogenous defence against infection for the success of antibiotic therapy is demonstrated using immune defect diseases as an example. The carriers of specific humoral defence against infection are the antibodies and the complement system. Acting either individually or in combination they result in neutralisation of toxins and viruses, an inflammatory reaction and the killing of pathogens. Humoral-cellular antibodies and the complement system play a role in phagocytosis, acting as phagocytosis-enhancing agents (opsonins). The possibility of interaction of antibiotic therapy and endogenous defence against infection is discussed.

Anti-Bacterial Agents↗
PubMed1988

Surface hydrophobicity and opsonic requirements of coagulase-negative staphylococci in suspension and adhering to a polymer substratum.

The opsonic requirements for phagocytosis in suspension of 38 clinical isolates of coagulase-negative staphylococci recovered from neonates with septicemia were found to be related to the degree of surface hydrophobicity of these strains. Sixteen isolates were adequately opsonized only in the presence of complement; this group was significant more hydrophobic (p less than 0.001) than the 22 strains not requiring complement for efficient uptake in suspension. Evidence showed that hydrophobic groups present on the bacterial surface may interfere with IgG opsonization. In contrast, IgG sufficed as an opsonin without complement being required for the efficient uptake of these hydrophobic strains when adhering to a polymer surface.

Bacterial Adhesion↗
PubMed1991

Antibacterial properties of breast milk: requirements for surface phagocytosis and chemiluminescence.

The opsonic components of breast milk responsible for phagocytosis of surface-adherent Staphylococcus aureus by human polymorphonuclear leukocytes were investigated. There was significantly greater phagocytosis of bacteria pre-opsonized with 100% breast milk than of unopsonized bacteria (p less than 0.001). Heat inactivation of breast milk had no effect on surface phagocytosis, indicating that phagocytosis is independent of complement. The predominant immunoglobulin in breast milk, secretory immunoglobulin A (IgA), did not promote phagocytosis. In contrast, IgG, which is present in very low amounts in breast milk (0.05 mg/ml), was as opsonic as 100% breast milk, suggesting that this is the major opsonin. An oxidative burst as measured by chemiluminescence was observed during phagocytosis of bacteria pre-opsonized with 100% breast milk. Heat inactivation of breast milk reduced the chemiluminescence response to the level of control. Neither secretory IgA nor IgG stimulated a polymorphonuclear leukocyte chemiluminescence response to surface-adherent bacteria. These experiments indicate that IgG is the principal component of breast milk responsible for surface phagocytosis but that complement is required for the generation of chemiluminescence and thus may be essential for intracellular killing of bacteria. Secretory IgA, despite its abundance in breast milk, has no effect on surface phagocytosis or neutrophil chemiluminescence.

Humans↗
PubMed1986

Regulation of macrophage phagocytosis.

The removal of pathogens from the circulation is achieved primarily by cells of the mononuclear phagocyte system, also known as the reticuloendothelial system. The tissue macrophage is the most important component of this system. The phagocytic activity of macrophages is regulated by opsonins on pathogenic materials and by endogenous cytokines. A number of diseases are caused by qualitative or quantitative disorders of phagocytosis by four major mechanisms: a decrease in the flow of blood to organs which contain macrophages (e.g. congestive heart failure and portal hypertension); a decrease in the quantity of tissue which contains macrophages (e.g. hepatic cirrhosis and splenectomy); a decrease in the effective opsonization of pathogens because of a deficiency of complement or IgG; and qualitative dysfunction of macrophages due to a deficiency of regulatory cytokines (e.g. gamma interferon and tuftsin) or a direct inhibitory effect on the macrophage (e.g. viral infections). New approaches for selective regulation of the phagocytic activity of macrophages are emerging.

Anemia, Sickle Cell↗
PubMed1981

Phagocytosis-promoting activity of avian plasma and fibroblastic cell surface fibronectins.

The purpose of this investigation was to determine whether fibronectin preparations from both chicken plasma and cell surface of fibroblasts can promote phagocytosis of gelatin-coated latex particles. Chicken plasma fibronectin was isolated (a) by ammonium sulfate fractionation, chromatography on Sepharose-4B followed by purification on a Sepharose-4B-heparin column; (b) by affinity chromatography on a Sepharose-4B-rat-antifibronectin column; (c) by affinity chromatography on Sepharose-4B-gelatin followed by molecular sieve separation on Sepharose-CL4B; (d) by a dual affinity chromatographic method using a Sepharose-4B-gelatin column and a Sepharose-4B-heparin column. Chicken cell surface fibronectin from fibroblast cultures was purified by ammonium sulfate precipitation followed by chromatography on Sepharose-CL4B. The purity of preparations was examined by polyacrylamide gel electrophoresis in the presence of sodium dodecylsulfate; all samples showing high purity. The opsonic activities of the preparations were measured by the uptake of 125I-labeled gelatin coated latex particles in conjunction with rat liver slice, and peritoneal macrophage monolayer systems. Both the plasma fibronectin and cell surface fibronectin preparations showed substantial opsonic activities in the test systems. Fresh chicken plasma did not reveal any phagocytosis promoting activity due to the presence of some unidentified inhibitor(s). The results showed that an opsonically active protein can be isolated from chicken plasma or serum and this protein is identical to plasma fibronectin. Furthermore, it could be concluded that cell surface fibronectin from chicken fibroblasts also can serve as an opsonin for gelatin coated particles.

Animals↗
PubMed1984

Pathogenic synergy: mixed intra-abdominal infections.

In this article we review our researches into the pathogenesis of mixed infections. These may conveniently be divided into in vitro and in vivo studies. In vitro we confirmed that interference with the killing of aerobes by polymorphonuclear leucocytes (PMN's) is a property of the Bacteroides strains tested and appears to depend on competition for opsonins i.e. complement factors. Further studies are in progress to define which complement factors and which bacterial structures are involved. The influence of B. fragilis on chemotaxis has also been studied. Our preliminary data suggest that B. fragilis is itself poorly chemotactic and reduces the chemoattractivity of Proteus mirabilis. This observation is surprising when we consider that abscess formation is the hall-mark of B. fragilis infections and needs clarification. In vivo we have developed a skin infection model in mice which is economical and gives reproducible and quantitative results. In this model we have demonstrated pathogenic synergy between Escherichia coli and B. fragilis. Further studies are planned to assess the role of complement and bacterial factors in this in vivo synergy.

Animals↗
PubMed2004

Opsonophagocytic dysfunction in patients with liver cirrhosis and low responses to tumor necrosis factor-alpha and lipopolysaccharide in patients' blood.

To evaluate their defense level against bacterial infection of patients with liver cirrhosis, we compared the luminol-dependent chemiluminescence (CL) response of peripheral blood from 40 patients with that from 40 healthy volunteers. Small quantities of heparinized whole blood (100 microl; final dilution, 1:10) were used for phagocytes, and CL was measured on addition of nonopsonized zymosan or Escherichia coli without special opsonization. Whole blood CL in cirrhotic patients was significantly lower than that in the healthy controls. The incidence of lower CL response in patients increased as disease stage advanced. Polymorphonuclear leukocytes (PMN) from cirrhotic patients exhibited a slightly lower CL response than those from controls, but this was not statistically significant. In contrast, the CL response of monocytes in patients was significantly lower than that of controls. The opsonizing capacity of the patients' sera and ascitic fluid was also decreased. In fact, the levels of opsonins such as complement in the patients' sera and both immunoglobulins and complement in the ascitic fluids were found to be lower in cirrhotic patients. On the basis of these findings, defect of opsonophagocytic function seems to participate in the increased susceptibility to infection in cirrhotic patients. Furthermore, whole blood CL induced by nonopsonized zymosan at the onset of relatively severe bacterial infections such as sepsis, pneumonia, or spontaneous bacterial infection was less augmented in the blood of cirrhotic patients than that in noncirrhotic patients. To clarify the reason why whole blood exhibits a lower CL response in the acute phase of bacterial infections, we investigated the priming effects of lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNF-alpha), well-known CL activators, on the CL response of whole blood obtained from cirrhotic patients in comparison with that from healthy persons. The priming effects were significantly decreased in patients' blood when compared with that of healthy persons. These low responses of patients' blood to LPS or TNF-alpha support our finding that phagocytes are not fully activated when gram-negative bacterial infections occur.

Adult↗
PubMed1983

Endocytosis by the mononuclear phagocyte system and autoimmune disease.

The mononuclear phagocyte system, formerly called the reticuloendothelial system, is an important element in basic immunology, cell biology, and clinical disease. Secretory products participate in inflammation and immunoregulation. Endocytosis mediated by specific receptors for immunoglobulin and complement or by other opsonins is important in removal of damaged self or foreign particles. The ability to assess receptor-specific endocytosis has led to the recognition of Fc-receptor dysfunction in certain autoimmune diseases. This defect in membrane receptor function, whether inherited or acquired, may be important in the pathogenesis of these diseases.

Animals↗
PubMed1984

Neutrophil chemi-luminescence and opsonic activities of young people with periodontitis in Thailand.

The polymorphonuclear neutrophils (PMN) produced significantly-higher chemi-luminescence (CL) peak values than neutrophils of healthy-paired controls when each population of cells was challenged with zymosan pre-opsonized with autologous serum. This enhanced CL was not attributable to the metabolic activity of the cells, but was shown, by cross-over experiments and additional testing with a single source of cells, to be directly associated with the opsonizing capacity of the patient's serum. The results suggest that peripheral PMN from young periodontitis patients have oxidative metabolic activities similar to subjects free of this disease, and that the enhanced PMN metabolism of patients may be due to a corresponding increase of serum opsonins.

Adult↗
PubMed1985

Respiratory infections may reflect deficiencies in host defense mechanisms.

Serious respiratory tract infections are rare in the healthy individual and most of the nuisance morbidity that occurs results from nasopharyngeal viral infections that many people get once or twice a year. The economic impact from these upper respiratory tract infections is appreciable, however, in terms of absenteeism from school or work, but unfortunately there is little that can be done to ward them off in a practical way. Pneumonia is an infrequent lifetime experience for most non-smoking adults and when it occurs, unusual circumstances may pertain--a particularly virulent microorganism is in circulation, or perhaps one has been exposed to a newly recognized germ, such as has occurred with Legionella species in the past 8 years or so. What protects us the great majority of the time is a very effective network of respiratory tract host defenses. These include many mechanical and anatomical barrier mechanisms concentrated in nose and throat; mucociliary clearance, coughing and mucosal immunoglobulins in the conducting airways and in the air-exchange region of the alveolar structures, phagocytes, opsonins, complement, surfactant and many other factors combine to clear infectious agents. The ability to mount an inflammatory response in the alveoli may represent the maximal and ultimate expression of local host defense. In some way these host defenses are combating constantly the influx of micro-organisms, usually inhaled or aspirated into the airways, that try to gain a foothold on the mucosal surface and colonize it. But many general changes in overall health such as debility, poor nutrition, metabolic derangements, bone marrow suppression and perhaps aging promote abnormal microbial colonization and undermine the body's defenses that try to cope with the situation. It is a dynamic struggle. The departure from normal respiratory health may not be obvious immediately to the patient or to the physician and repeated episodes of infection or persisting symptoms of cough, expectoration and sinus or ear infections may develop before serious assessment of the situation is taken and appropriate diagnosis gotten underway. Obvious explanations for respiratory infections may be apparent and, nowadays, side effects from antineoplastic chemotherapy or immunosuppressive therapy for a variety of diseases that create an immunocompromised host are common. In a few subjects, especially young adults who present with a cumulative history of frequent but mild infections in childhood and youth, a subtle deficiency in host defenses may exist and have been partially masked because of attentive pediatric medical care and prompt use of broad spectrum antibiotics.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1977

Kinetics of staphylococcal opsonization, attachment, ingestion and killing by human polymorphonuclear leukocytes: a quantitative assay using [3H]thymidine labeled bacteria.

A method has been developed for studying quantitatively the separate processes of bacterial opsonization, phagocytosis, and killing by human polymorphonuclear leukocytes using [3H]thymidine labeled Staphylococcus aureus. Phagocytosis is determined by assaying for leukocytes-associated radioactivity after differential centrifugation and washing the leukocytes. Opsonization is studied by incubating bacteria with an opsonic source for varying durations and then adding leukocytes. By treatment of samples with the muralytic enzyme, lysostaphin, the attachment and ingestion phases of phagocytosis can be separated. Sampling for colony forming units after disruption of the leukocytes permits the measurement of bacterial killing. Using this method, differences in the kinetics of staphylococcal opsonization by normal and C2 deficient sera were defined, opsonic influences on the attachment and ingestion phases of pH agocytosis were delineated, and the influences of different opsonins and leukocyte populations on killing were determined.

Blood Bactericidal Activity↗
PubMed1986

A quantitative fluorescent method for measurement of bacterial adherence and phagocytosis.

We have developed a new two-color fluorescent method for the quantitative measurement of adherence and ingestion of Streptococcus pneumoniae by human monocytes. The method employs a fluorescent naphthalimide, Lucifer Yellow VS, that has been covalently linked to the bacterial cell wall. Bacteria were opsonized and allowed to adhere to monocytes. Lucifer Yellow did not alter the bacterial interaction with complement in serum or with the phagocytic cell. The ability of monocytes to ingest the adherent bacteria was tested under a variety of conditions. Rabbit antibody to Lucifer Yellow derivatized with Texas Red was used to detect monocyte-bound, but uningested bacteria. Dual laser flow cytometry simultaneously quantitated the total number of monocyte-associated S. pneumoniae and the number that remained surface adherent. This method allows separate analysis of the opsonins and receptors involved in bacterial adherence to phagocytes and in the ingestion process.

Adhesiveness↗
PubMed1989

A rapid turbidimetric assay of phagocytosis and serum opsonizing capacity.

An in vitro assay has been developed to measure the opsonizing capacity of serum and the extent of bacterial uptake by phagocytes. Various micro-organisms were preopsonized for 10 min with a serum concentration previously determined to be optimal for the respective types of micro-organism. Subsequently, neutrophils from a healthy donor were added to the preopsonized bacteria in a cuvette of a spectrophotometer. The decrease in turbidity at 400 nm, resulting from the uptake of the micro-organisms by the neutrophils, was measured for 20-30 min and the area under the curves was taken as a measure of the opsonizing capacity of the serum or the phagocytic capacity of the neutrophils. The results correlated well with standard opsonophagocytic assays. By excluding Ca2+ from the buffer of the assay, phagocytosis was distinguished from the combined response of phagocytosis and aggregation. In the presence of Ca2+ ions, both phagocytosis and aggregation contributed to the decrease in turbidity. In the absence of Ca2+, phagocytosis was normal, but aggregation was completely inhibited. Phagocytosis in the absence of Ca2+ was also observed using microscopic and radiometric methods of evaluation. Neutrophils from a patient with a deficiency of leukocyte adhesion molecules, ingested as many bacteria as did normal neutrophils without Ca2+. Experiments with NaF, to inhibit phagocytosis, indicated that the change in turbidity measured in the absence of Ca2+ was mainly caused by phagocytosis, not by attachment of bacteria to the neutrophils. The opsonizing capacity of sera, as determined in our assay, depended both on antibodies and on an intact complement system and the inter-assay variance was less than 5%. We found a close correlation between turbidity changes measured in the presence or absence of Ca2+, suggesting that both phagocytosis and aggregation are opsonin-dependent. This assay is applicable to a variety of opsonizing fluids and micro-organisms, and can be used for assessing the phagocytic capacity of patients' neutrophils as well as for assessing the opsonizing capacity of patients' sera.

Blood Bactericidal Activity↗
PubMed1991

Ontogeny of fetal sheep polymorphonuclear leukocyte phagocytosis.

Premature infants and neonates are vulnerable to bacterial sepsis. This susceptibility may be due to the relative immaturity of their immune systems. To determine if neonates and, in particular, premature infants have decreased polymorphonuclear leukocyte (PMN) phagocytosis, we tested PMN phagocytosis of Staphylococcus aureus as a function of gestational age in the fetal lamb model. Because phagocytosis is made more efficient by the presence of opsonins in plasma, fetal and postnatal PMN phagocytosis were also measured after exposure to fetal and adult plasma. PMNs were isolated from fetal lambs at 104, 114, 124, and 141 days' gestation (term gestation for the fetal lamb is 145 days), as well as from 10-day-old neonatal sheep and adult sheep. Labeled S aureus were opsonized by incubation in either fetal or adult plasma, or left unopsonized for baseline values. Phagocytosis was measured as a percent of adult PMN phagocytosis after adult plasma opsonization. It was found that fetal PMN function is limited by two factors during the early third trimester: a primary defect in the ability of the PMN to phagocytose S aureus despite adequate opsonization, and the diminished ability of autologous fetal plasma to opsonize bacteria. The defect in PMN phagocytosis disappears late in the third trimester, but the inability of the fetal plasma to opsonize effectively continues until after birth.

Age Factors↗