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PubMed1993

Hemolytic function of opsonizing proteins of earthworm's coelomic fluid.

Synthetic 2-hydroxyethylmethacrylate copolymer particles (HEMA) can be opsonized in the coelomic fluid of Eisenia foetida earthworms. The incomplete coelomic fluid (i.e., the coelomic fluid after incubation with HEMA particles) exerts a lower level of hemolytic activity compared to complete coelomic fluid. The decreased hemolysis can be compensated by the addition of isolated opsonins. On the other hand, isolated opsonins do not possess direct hemolytic capacity. It can be suggested that at least one of the isolated opsonins is involved in the hemolytic process. These results support the hypothesized cooperation of humoral and cellular mechanisms in earthworm defence.

Animals↗
PubMed2000

Opsonophagocytosis versus lectinophagocytosis in human milk macrophages.

Some important immunoprotective effects of human breast milk have been attributed to the presence of macrophages. We investigated the generation of superoxide anion (O2-) by monocytes and human milk macrophages after stimulation with opsonized and unopsonized zymosan in the absence and presence of mannose as an inhibitor to investigate lectinophagocytic and opsonophagocytic properties. Peripheral blood monocytes generated more O2- than human milk macrophages (417,4 + 79,1 nmol O2-/mg protein vs. 216,1 +/-15,1 nmol O2-/mg protein, p<0,05) after stimulation with opsonized zymosan. When unopsonized zymosan was used as a serum-independent stimulus monocytes generated slightly less O2- in comparison to human milk macrophages (150,8 +/- 34,5 nmol/mg protein vs. 176,1 +/- 18 nmol O2-/mg protein, p<0,05). These findings demonstrate that the proportion of opsonin-independent phagocytosis in human milk macrophages is higher than in monocytes (82% vs. 36%). When mannose was used as an inhibitor a significantly higher reduction of O2- generation occurred in human milk macrophages compared to monocytes stimulated with opsonized zymosan, whereas no difference was found when unopsonized zymosan was used. These results indicate that human milk macrophages are stimulated to a greater extent by opsonin-independent mechanisms than blood borne monocytes. As the colostrum and the intestinal environment of the neonate offers only a little amount of opsonins like complement and immunoglobulin G, such a differentiation to lectinophagocytic properties could bear a great advantage for protective functions of human milk macrophages.

Adjuvants, Immunologic↗
PubMed1989

[Insufficiency of intra-abdominal immunity to infection in purulent peritonitis--sequela of disordered foreign body opsonization].

Despite a high concentration of serum proteins and intact phagocytes peritonitis exudates contain a large number of viable, pathogenic bacteria. The reason for this biological paradox is unknown. Our investigations reveal a pronounced defect in humoral opsonization of foreign particles in peritonitis exudate. We evaluated a modified chemiluminescence system allowing the determination of opsonic activity in serum and exudate. In serum we found a close correlation between opsonic activity and immunologically measurable levels of C3-complement and IgG. In purulent peritonitis exudates, however, the actual opsonizing activity was much less than expected according to the opsonin concentrations. We found a pronounced difference between immunologically determined opsonin levels and impaired opsonic function. Employing crossed immunoelectrophoresis massive C3-splitting into smaller fragments could be demonstrated in peritonitis exudates. In these exudates we found very high concentrations of granulocyte proteolytic (elastase) and oxidative (myeloperoxidase) enzymes which may lead to a functional destruction of opsonins followed by impaired opsonization in peritonitis exudate. The great number of bacteria and foreign particles in addition can cause a pronounced physiological consumption of complement components. The almost complete breakdown of intact C3-complement in intraabdominal exudate explains the deficient host defence in patients with severe peritonitis.

Bacterial Infections↗
PubMed1992

Opsonophagocytosis of liposomes by peritoneal macrophages and bone marrow reticuloendothelial cells.

We investigated the opsonic effect of serum on the phagocytosis of cholesterol-poor and cholesterol-rich liposomes with freshly prepared rat bone marrow and peritoneal phagocytes in suspension. The presence of serum in incubation increased the uptake of cholesterol-rich but not cholesterol-poor liposomes in bone marrow cells, whereas serum enhances phagocytosis of both liposome preparations in peritoneal phagocytes. The opsonic activity of serum on the uptake of liposomes by both cell types is destroyed by heat, ammonium hydroxide, and zymosan treatments of serum, which suggests the involvement of complement in phagocytosis of liposomes. However, bone marrow cells and peritoneal macrophages responded differently when incubated with dialysed or EGTA-chelated serum. These treatments result in complete loss of the opsonic effect of serum on the uptake of liposome in bone marrow cells. Addition of serum dialysate or divalent cations to dialysed serum do not reinstall its lost opsonic activity. Thus these results shade doubt on possibility of involvement of complements in phagocytosis of liposomes by bone marrow cells. Dialysed or EGTA-treated serum also failed to promote liposome uptake by peritoneal macrophages but unlike in the case of bone marrow cells replacement of divalent cations to such sera reinstalls its opsonic activity and enhances phagocytosis of liposomes by peritoneal macrophages. These observations suggest the involvement of different serum components on liposome uptake by bone marrow cells and peritoneal macrophages, and emphasize the complexities associated with RES-mediated blood clearance of the intravenously injected liposomes. The properties of these opsonins are compared with those of 'liver-' and 'spleen-specific' opsonins responsible for phagocytosis of liposomes by Kupffer cells and spleen macrophages, respectively [4]. It is suggested that these tissue specific opsonins are responsible for distribution of intravenously injected liposomes in various organs of the reticuloendothelial system.

Ammonium Hydroxide↗
PubMed2006

Efficient clearance of opsonised apoptotic cells in the absence of PECAM-1.

It is now accepted that the recognition and uptake of apoptotic cells by phagocytes is a complex process involving a large number of opsonins, receptors and ligands, however the relative contribution of all these molecules are still debated. Here we examined the role of CD31 (PECAM-1) in the recognition/uptake of apoptotic thymocytes by murine bone marrow-derived macrophages (BMDM) in vitro, and by resident peritoneal macrophages in vivo. In the absence of serum, CD31 deficiency, on either the phagocyte or the apoptotic cell, resulted in a reduction in the clearance of apoptotic thymocytes, when a high ratio of apoptotic cells to macrophages was applied. In the presence of serum however there was no discernible contribution of CD31 to the clearance of apoptotic cells by bone marrow-derived macrophages, irrespective of the ratio of cells used. In vivo peritoneal clearance experiments confirmed that in the presence of soluble opsonins CD31 deficiency had no effect on this process. These data suggest that the overall role played by CD31 in the ingestion of apoptotic cells is negligible and most likely overwhelmed by the effects of serum opsonins, such as complement components.

Animals↗
PubMed1994

Opsonophagocytosis in infected urine: relation to pH and osmolality.

Polymorphonuclear neutrophils (PMN) in freshly voided urines from 20 symptomatic bacteriuric patients were examined. Although the PMN were viable (median 85%), in only 2 cases could phagocytosis of the infecting organisms be demonstrated, even after the addition of serum opsonins. Polymorphonuclear neutrophils from urines of 12 patients were also unable to phagocytose added opsonized Staphylococcus aureus. These urines were found to be of pH < 6.0 and/or osmolality > 700, or < 180 mOsm. However, the phagocytic function of these PMN was restored when transferred to Hanks balanced salt solution (HBSS). By contrast, most PMN in urines of suitable pH (> or = 6.0) and osmolality (between 200 to 700 mOsm.) phagocytosed the opsonized S. aureus. When bacteria cultured from the infected urine were incubated in the same urine and then transferred to HBSS, in 17 of 19 cases opsonization occurred and the organisms were phagocytosed when PMN, isolated from blood, were added. IgG appeared to be the prime opsonin in the urines, and heat-stable opsonins for S. aureus were also present. It is concluded that lack of opsonization is not a major cause of the absence of phagocytosis by urinary PMN. Low pH and adverse osmolality are largely responsible, correction of which may restore PMN function in vivo.

Antibody-Coated Bacteria Test, Urinary↗
PubMed2002

Liposome clearance.

The clearance rate of liposomal drugs from the circulation is determined by the rate and extent of both drug release and uptake of liposomes by cells of the mononuclear phagocyte system (MPS). Intravenously injected liposomes initially come into contact with serum proteins. The interaction of liposomes with serum proteins is thought to play a critical role in the liposome clearance. Therefore, in this review, we focus on the role of serum proteins, so-called opsonins, that enhance the clearance of liposomes, when bound to liposomes. In addition to opsonin-dependent liposome clearance, opsonin-independent liposome clearance is also reviewed. As opposed to the conventional (non-surface modification) liposomes, we briefly address the issue of the accelerated clearance of PEGylated-liposomes (sterically stabilized liposomes, long-circulating liposomes) on repeated injection, a process that has recently been observed.

Animals↗
PubMed1975

Humoral mediated macrophage response during tumour growth.

Reticuloendothelial (RE) phagocytic and circulating plasma opsonic activity was evaluated in rats transplanted with the Walker 256 carcinoma tumour in an attempt to evaluate the role of opsonic protein in governing the functional state of the macrophage system. Animals transplanted intramuscularly with 2 X 10(4) viable tumour cells manifested 2 peaks of RE stimulation at 6 and 14 days post-transplantation with a subsequent decline in the phagocytic activity over the 14-30 day period. Increased phagocytic activity as determined by colloid clearance was primarily a reflection of hepatic Küpffer cell hyperphagocytosis while the decline in phagocytic activity was related to a decrease in Küpffer cell function. The initial peak of RE stimulation was associated with an elevation in the blood opsonin level and no significant enlargement of the liver and spleen. In contrast, the second peak of RE stimulation at 14 days was associated with both an elevation in opsonin levels and an associated hepatic and splenic enlargement. The decline in phagocytic activity over the 14-30 day interval was associated with a progressive decline in the plasma opsonic activity, a return of the spleen to its normal size in relationship to the body weight, and a persistent hepatomegaly. These findings suggest that the alterations in macrophage function during tumour growth may be mediated in part by changes in the opsonic or phagocytosis promoting capacity of plasma. Since opsonic protein contributes to the discriminatory capacity of macrophages, it is suggested that changes in the blood opsonin level may condition the anti-tumour capacity of the macrophage system with respect to host defence aginst malignant disease.

Animals↗
PubMed1997

Colostral mononuclear phagocytes are able to kill enteropathogenic Escherichia coli opsonized with colostral IgA.

Enteropathogenic Escherichia coli (EPEC) is the main aetiological agent of acute diarrhoea among low socioeconomic level infants in developing countries. Breast-feeding provides infant protection against acute gastrointestinal and respiratory infections; however, little is known about the protective role of colostral phagocytes in the gut of newborn infants. In the present investigation we studied the ability of human colostral MN phagocytes to kill EPEC as well as the interactions between these cells and colostral and serum opsonins. The authors observed that the microbicidal activity of colostrum MN phagocytes was dependent on previous EPEC opsonization with colostral supernatant or blood serum. A defatted colostrum supernatant pool presented opsonic activity for EPEC killing at levels equivalent to those of normal serum. IgA-depleted colostrum supernatant showed significantly lower opsonic activity, whereas purified IgA from the same colostrum pool was a potent opsonin which induced EPEC killing at levels equivalent to those of untreated colostrum. Colostral MN phagocytes are able to release superoxide anion when incubated with both EPEC opsonized with untreated colostrum and purified IgA. Purified IgA was also able to restore opsonic activity of IgA-depleted colostrum. A colostrum pool without C3 and IgG induced EPEC killing by colostral MN phagocytes at rates equivalent to those of untreated colostrum supernatant. Addition of an IgM MoAb (My43) anti-human Fc alpha receptor resulted in a significant inhibition of EPEC killing when bacteria were opsonized with purified IgA, suggesting an interaction between IgA and Fc alpha R. With respect to serum opsonins, we observed that IgG plus complement component C3 were necessary to induce EPEC killing by the colostrum MN phagocytes. Colostral phagocyte killing of enteropathogenic bacteria may represent an additional mechanism of breast-feeding protein against intestinal infections during the first week of life.

Adolescent↗
PubMed1980

Mechanism for pulmonary protection by lipopolysaccharide pseudomonas vaccine.

Recent studies in guinea pigs indicated that active vaccination with a cell wall-derived, lipopolysaccharide (LPS) pseudomonas vaccine confers specific protection against acute pneumonia. This study analyzed the immune mechanisms by which LPS pseudomonas vaccine offers local protection to the lung. Neither parenteral vaccination nor direct exposure of lung tissues to living Pseudomonas activated alveolar macrophages. However, serum opsonic activity that specifically enhanced phagocytosis of Pseudomonas by alveolar macrophages was significantly increased (P < 0.05) in vaccinated animals. Serum pseudomonas opsonins were heat-stable but were sensitive to reduction of macroglobulins by 2-mercaptoethanol. Within 3 hr after establishment of experimental pseudomonas pneumonia, a fourfold increase in local pseudomonas opsonins was found in bronchial fluids from vaccinated animals, presumably secondary to diffusion of serum proteins into local inflammatory fluids. Thus, Pseudomonas-specific opsonic antibody appears necessary to augment alveolar macrophage phagocytosis after LPS vaccination, and local vaccination of the respiratory tract is not required to provide adequate local pseudomonas opsonins during acute pneumonia.

Animals↗
PubMed1985

Serum factors for opsonisation of non-typable Haemophilus influenzae.

Neutrophil chemiluminescence was used to assess the opsonins required for phagocytosis of non-typable Haemophilus influenzae isolated from sputum samples of patients with hypogammaglobulinaemia. Immunoglobulin was the major opsonin, whereas complement was relatively unimportant. Evidence was found for a heat-labile opsonin other than complement that enhanced phagocytosis of these organisms. Tuftsin was shown to aid phagocytosis of H. influenzae without triggering chemiluminesence.

Agammaglobulinemia↗
PubMed1990

Opsonic requirements and surface hydrophobicity of novobiocin-resistant, coagulase-negative staphylococci.

The opsonic requirement for phagocytosis and killing and cell-surface hydrophobicity of five strains of Staphylococcus saprophyticus isolated from clinical sources were studied. Phagocytosis and killing of bacteria by human granulocytes were measured in suspension. Bacterial aggregating cell-surface hydrophobicity was determined by salt aggregation, and the absorptive hydrophobicity was measured by hydrophobic interaction chromatography. All strains were well opsonised by pooled normal human serum 10%. Ingestion of these bacteria could be detected to a variable extent in the absence of extracellular opsonins; heat-inactivated serum 10% or intravenous IgG concentrate 1 mg/ml improved phagocytosis of all strains. Significantly increased rates of both the ingestion and killing of one of the five strains occurred in the presence of IgG or in the absence of opsonins, compared to those found with each of the other four. This particular strain had significantly stronger adsorptive surface hydrophobicity than the other four strains, and with all strains there was a correlation between hydrophobicity and phagocytosis by granulocytes in the absence of opsonins.

Coagulase↗
PubMed1989

Surface phagocytosis of Staphylococcus epidermidis and Escherichia coli by human neutrophils: serum requirements for opsonization and chemiluminescence.

We examined the serum requirements for surface phagocytosis of Staphylococcus epidermidis and Escherichia coli and for the subsequent chemiluminescent response of human neutrophils. Substantial surface phagocytosis of S. epidermidis occurred in the absence of opsonins, although the presence of 10% pooled or heat-inactivated serum significantly increased phagocytosis. There was no significant difference between these opsonins, indicating that surface phagocytosis of S. epidermidis did not require complement. Unopsonized E. coli were not as readily phagocytized as S. epidermidis (33% versus 57%). In contrast to S. epidermidis optimal phagocytosis of E. coli required complement as 10% heat inactivated donor serum (HHS) was significantly less effective as an opsonin than 10% pooled healthy donor serum (PHS). The time kinetics for phagocytosis of each organism were similar, with most of the phagocytosis occurring in the first 10 min. The chemiluminescent response of neutrophils produced discrepant results. Maximal chemiluminescence was observed when neutrophils were stimulated with bacteria opsonized in PHS. The response to HHS-opsonized bacteria was less, and chemiluminescence to unopsonized bacteria was only marginally higher than the control, even though there was relatively good phagocytosis. These results define the opsonic requirements for surface phagocytosis of S. epidermidis and E. coli and indicate that although complement may not be required for phagocytosis, it is necessary for generation of a maximal oxidative burst, and thus may be essential for efficient intracellular killing.

Blood Bactericidal Activity↗
PubMed2000

Opsonization of apoptotic cells. Implications for uptake and autoimmunity.

As a part of innate immunity, soluble host proteins called opsonins, which include complement ligands and immunoglobulins, initially coat microorganisms that penetrate the mammalian sterile milieu. The main purpose of opsonization is to allow subsequent clearance of opsonized particles by specific receptors on the surface of leukocytes. Similarly, several proteins that may act as opsonins and have a role in uptake of apoptotic cells and bodies include thrombospondin I, the complement system, beta 2GPI, immunoglobulins, CRP, and some unidentified others. The surface changes that lead to opsonization include the appearance of phosphatidylserine that acts as an activator molecule for some known opsonins as the complement system and beta 2GPI. The consequence of altered opsonization is demonstrated by the development of autoimmunity in C1q deficient mice, and the pro-inflammatory response by macrophages ingesting apoptotic cell opsonized by an autoantibody.

Animals↗
PubMed1978

Stimulation of polymorphonuclear leukocyte bactericidal activity by supernatants of activated human mononuclear cells.

Supernatants of phytohemagglutinin-activated human mononuclear cells stimulated polymorphonuclear leukocyte (PMN) activity against the gram-negative organism Serratia marcescens. In the absence of serum opsonins, when control PMN could not impede bacterial growth, stimulated PMN averaged more than 0.6-log kill of the original bacterial inoculum. In the presence of optimal amounts of serum opsonins, when control PMN were significantly bactericidal, stimulated PMN killed, on the average, at least 0.6 log more of bacteria. Stimulation was not found when PMN were preincubated with supernatants for 1 h or less. The data strongly suggested that the action of the PMN stimulating factor was independent of and different from classically described serum opsonins. PMN stimulating activity may be an additional lymphokine-mediated immune defense mechanism enabling hosts to kill invading microorganisms.

Antibodies↗
PubMed1979

Influence of encapsulation on phagocytosis of Pasteurella multocida by bovine neutrophils.

The effect of encapsulation on phagocytosis of Pasteurella multocida by bovine neutrophils was examined by using two encapsulated strains, NA77 (capsular type A) and C42 (capsular type B), and comparing them with an unencapsulated counterpart strain, 1173. The uptake of [(3)H]thymidine-labeled bacteria by neutrophils was quantitatively measured after incubation of the bacteria in normal bovine serum, heat-inactivated serum, and hyperimmune sera (anti-NA77 and anti-C42). Results showed that all three strains of P. multocida were ineffectively opsonized by the heat-labile serum complement system. The unencapsulated strain was completely phagocytized in the presence of heat-stable opsonins found in normal serum. Although encapsulation of strain C42 was found to interfere with opsonization by normal serum, this strain was completely phagocytized when hyperimmune serum (anti-C42) was used as the opsonin source. These results suggest that specific anticapsular antibodies found in the hyperimmune serum readily opsonized the encapsulated strain C42 and enhanced phagocytosis. The presence of a thick capsule on strain NA77 interfered with phagocytosis in the presence of normal or hyperimmune serum (anti-NA77). This interference was due to the presence of hyaluronic acid which was a major component of the capsule. Treatment of this encapsulated strain with hyaluronidase decapsulated the bacteria. Bacteria treated in this way were almost completely phagocytized (90%) in the presence of heat-stable opsonins. The exact mechanism by which the capsule of P. multocida NA77 interfered with phagocytosis was not demonstrated; perhaps the slimy nature of the hyaluronic acid makes the phagocytic act difficult by changing the physiochemical surface properties, or it may prevent opsonization.

Animals↗
PubMed1996

Entry and intracellular survival of group B streptococci in J774 macrophages.

The mouse macrophage-like cell line J774 was used to analyze opsonin-independent entry and survival of group B streptococci (GBS). Efficient entry of GBS in J774 cells occurred within 5 min postinfection, and streptococci persisted intracellularly without loss of viability for at least 8 h. At 24 h postinfection, 30% of the total intracellular GBS was recovered from macrophages. Inhibition studies using different biochemical modulators of cellular functions showed that bacterial entry seemed to involve nonglycosylated J774 surface structures different from known receptors such as fibronectin-binding integrins. Internalization of GBS by J774 cells occurred by a microfilament-dependent phagocytosis-like process also involving participation of receptor-mediated endocytosis. Prior opsonization of GBS with human serum containing anti-GBS antibodies did not affect bacterial entry but significantly reduced the intracellular survival of GBS. Transmission electron microscopic analysis confirmed these findings and demonstrated that both opsonized and nonopsonized bacteria were contained within phagosomes during the whole infection period. Transmission electron microscopy further revealed that decreased intracellular survival rates of opsonized GBS appeared to be due to increased lysosomal activities of the macrophages. These results suggest that in the absence of opsonins, GBS are able to enter and persist efficiently in macrophages by evading intracellular antibacterial activities commonly associated with opsonin-mediated uptake.

Animals↗
PubMed1997

Identification of phosphatidylinositol mannoside as a mycobacterial adhesin mediating both direct and opsonic binding to nonphagocytic mammalian cells.

The molecular basis for the binding of Mycobacterium tuberculosis to nonphagocytic cells, which are readily infected in vitro, and the in vivo significance of this interaction are incompletely understood. Of six cell types tested, we found that only two, Chinese hamster ovary (CHO) fibroblasts and primary porcine aortic endothelial cells, were able to bind M. tuberculosis H37Rv efficiently in vitro. Binding to both CHO and endothelial cells was markedly (three- to fivefold) enhanced by 10 to 20% human or bovine serum, suggesting that the bacteria were coated by a serum opsonin. Preincubation with individual candidate opsonins revealed that recombinant human mannose-binding protein (rMBP), fibronectin, and transferrin were each able to enhance binding threefold. Preincubation of bacteria in serum depleted of mannan-binding lectins or in genetic MBP-deficient serum resulted in enhancements that were only approximately 60 and 58%, respectively, of that produced by preincubation in control serum. In contrast, serum depleted of fibronectin or transferrin retained its opsonizing capacity, suggesting that the latter two are not significant opsonins in whole serum. Binding of M. tuberculosis and Mycobacterium smegmatis to both CHO and endothelial cells in the presence or absence of serum was blocked (60 to 70%) by a monoclonal antibody, MAb 1D1, selected for recognition of intact bacilli. The 1D1 antigen was purified from mycobacterial cell walls and chemically identified as a polar phosphatidylinositol mannoside (PIM). Latex beads coated with purified 1D1 antigen bound to CHO cells, which was enhanced threefold by serum and abolished by periodate treatment, suggesting a requirement for the PIM mannoses in opsonic adhesion. This was likely mediated, at least in part, by serum MBP, as rMBP bound strongly to 1D1 antigen in both thin-layer chromatography overlay and plate binding assays, the latter in a mannan-inhibitable manner. This is the first demonstration that mycobacterial PIMs can function as adhesins for binding to nonphagocytic cells, both directly and after opsonization with serum proteins, including MBP.

Adhesins, Bacterial↗