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Biological characteristics of the Calliphora vomitoria agglutinin.

The galactose specific agglutinin from Calliphora vomitoria was found to be expressed in the haemolymph of all the larval instars, but could not be detected at any other time during the life cycle. The haemagglutinating activity was insensitive to wounding of the tegument or injection of saline; however, a significant increase in haemagglutinating titre could be induced upon inoculation of the haemocoel with biotic or abiotic particulate material. The agglutinin also actively agglutinated several bacterial species and appeared capable of playing a role in particle--haemocyte interaction. The presence of the purified agglutinin significantly increased the attachment of fetuin-derivatized beads to haemocytes in vitro, and this activity could be specifically reduced by the addition of galactose, suggesting that the agglutinin may act as an opsonin.

Animals↗
PubMed1988

Differing complement-mediated opsonic activity of rabbit interstitial fluids from autologous serum.

Lack of appropriate methods for withdrawing extravascular or interstitial fluid from an animal host has limited in vitro study on the role of complement in the local defence of the extravascular space. In the present study, we obtained fluids from membrane diffusion chambers (porosity 0.22 micron) implanted into the kidneys, peritoneal cavity and soft tissues in rabbits. The complement-mediated opsonic activity (CMOA) of these fluids for Staphylococcus aureus ATCC 502A and Escherichia coli 01 was then compared to that of autologous sera. Soft tissue and renal interstitial fluids were as opsonic for E. coli as autologous sera but were however, poor opsonins for S. aureus. The peritoneal fluid was marginally effective in opsonization of both bacterial strains. While chelation of the fluids with MgEGTA (to block the classical pathway) did not diminish CMOA for E. coli, it reduced the CMOA for S. aureus by half. Conversely, heat-inactivation of the fluids and serum eliminated the opsonic activity for E. coli but only decreased the opsonic activity for S. aureus by half. Following a 24 h in vivo growth of E. coli in the implanted chambers, the CMOA was drastically reduced. Concomitant to the reduction in functional complement in the fluids, E. coli recovered from the chambers were found coated, though not maximally, with C3b as evidenced by studies with fluorescent antibody. The differences in opsonic content of extravascular fluids observed here might explain why certain sites of the body may be more vulnerable to attack by some bacterial species which are not effectively opsonized and therefore phagocytized.

Animals↗
PubMed1987

Neutrophil phagocytic and serum opsonic response of the foal to Corynebacterium equi.

This study was undertaken to examine the neutrophil response to Corynebacterium (Rhodococcus) equi, and to assess the possibility of neutrophil immaturity or malfunction in predisposition to C. equi pneumonia in foals. Neutrophil phagocytosis of Corynebacterium (Rhodococcus) equi was studied in foals from birth to 6 months of age. Chemiluminescence (CL) and bactericidal assays were used to assay the phagocytic response of peripheral blood neutrophils to C. equi in vitro. Results of in vitro bactericidal and CL assays indicate that foal neutrophils are able to ingest and kill C. equi, however are significantly more efficient in the presence of opsonization with specific antibody, and less importantly complement. Neutrophil CL was significantly decreased (p greater than .05) or eliminated by antibody adsorption, heat-inactivation, or removal of serum from the assay. The ability of the neutrophil to kill C. equi, as measured by in vitro bactericidal assay, was greater than 90% killing by 6 hours, in the presence of C. equi antiserum. Bactericidal activity was reduced to less than 40% killing when C. equi adsorbed serum was used as the opsonin source. As CL results indicated complement involvement in the opsonization of C. equi, the temporal development of hemolytic and conglutinating complement was measured in normal and C. equi infected foals. Neither defects nor age-related suppression of neutrophil function or complement activity were detected in C. equi affected foals, suggesting that these are not pathogenic mechanisms involved in foal pneumonia.

Animals↗
PubMed1992

Identical point mutation leading to low levels of mannose binding protein and poor C3b mediated opsonisation in Chinese and Caucasian populations.

A common opsonic defect occurring in 7% of the Caucasian population is associated with low serum levels of the lectin mannose binding protein (MBP). This study sought to determine whether the deficiency was also present in a Chinese population using sera obtained from 100 healthy Chinese children (age range 6 weeks-16 years). The distribution profiles of MBP levels and C3b/C3bi fragments binding to mannan coated plates were both bimodal and similar to the corresponding Caucasian profiles. Serum MBP levels were low in 9% of the Chinese children and all of these sera generated low levels of C3b/C3bi fragments. Overall there was a high significant correlation between MBP levels and C3b opsonin generation (r = 0.77; P less than 0.001). By analogy with similar findings in a Caucasian population we believe this correlation to be a reflection of antibody independent complement activation by MBP. In a pilot study of DNA obtained from three adult Chinese with low MBP levels the point mutation causing MBP deficiency in Caucasians was identified in all three cases.

Adolescent↗
PubMed1989

Opsonization of normal myelin by anti-myelin antibodies and normal serum.

Fc receptor-dependent myelin phagocytosis has been proposed as a possible important effector mechanism in several immune-mediated demyelinating diseases. The present study was designed to determine whether myelin is opsonizable by anti-myelin antibodies. Thioglycolate-elicited mouse peritoneal macrophages were cultured with 125I-labelled bovine central myelin pretreated with normal or immune serum. Serum opsonic activity was determined by a kinetic study comparing macrophage uptake of opsonized and untreated 125I-myelin. Heat-stable and heat-labile myelin opsonins were detected in normal rabbit serum. Myelin was also opsonized by normal rabbit gamma globulin and by heat-inactivated normal mouse, human, and guinea pig serum. Increased opsonic activity was detected in rabbit anti-myelin antiserum and the gamma globulin fraction prepared from this serum, in anti-myelin basic protein and anti-galactocerebroside antiserum but not in anti-myelin-associated glycoprotein antiserum or in serum from rabbits injected with Freund's adjuvant alone. One out of three anti-sheep red blood cell antisera tested also showed increased myelin opsonic activity. It is concluded that anti-myelin antibodies can promote opsonic phagocytosis, and that normal serum and normal serum gamma globulin also opsonize myelin.

Animals↗
PubMed1993

Coating particles with a block co-polymer (poloxamine-908) suppresses opsonization but permits the activity of dysopsonins in the serum.

The surfaces of polystyrene microspheres (60 nm in diameter) and colloidal gold particles (17 nm in diameter) were coated with a polyoxyethylene (POE)/polyoxypropylene (POP) block co-polymer; poloxamine-908. The polymer adsorb strongly to the microspheres via its relatively hydrophobic POP segments. This leaves the POE chains in a mobile state as they extend outward from the surface and thereby provide stability to the particle suspension by suppressing aggregation. The blood clearance and biodistribution of uncoated vs. poloxamine-908-coated 125I-labelled polystyrene microspheres were compared 1 h after intravenous administration into rats. Poloxamine coating dramatically reduced liver accumulation of microspheres and kept them within the systemic circulation. These observations were further confirmed by electron microscopy, demonstrating that Kupffer cells were loaded with uncoated latex but had ingested few if any of the poloxamine-908-coated particles. The interaction of uncoated and poloxamine-coated gold particles with freshly isolated rat liver sinusoidal cells was examined by electron microscopy. The accumulation in Kupffer cells of gold particles after opsonization with autologous plasma was in accordance with previous observations where the dominant opsonizing activity had been identified as fibronectin. In contrast, coating of gold particles with poloxamine-908 prior to plasma opsonization prevented the adsorption of fibronectin onto their surface. Simultaneously, Kupffer cells failed to recognize poloxamine-908-coated gold particles before and after opsonization. Unlike Kupffer cells, liver endothelial cells endocytosed poloxamine-908-coated gold particles prior to opsonization but failed to recognize them after the opsonization process. This was taken as an indication of the presence of dysopsonic activity in plasma. This dysopsonic activity was studied using polystyrene latex microspheres, where the uptake of such particles by phagocytes is known to be independent of opsonization. The coating of 125I-labelled polystyrene microspheres with poloxamine-908 dramatically reduced their interaction with liver sinusoidal cells. This interaction was further reduced in the presence of either autologous plasma or serum. A heat-stable (60 degrees C for 15 min) serum component of molecular mass > 100 kDa was found to mediate this suppressive effect. Thus, we demonstrate that organ-specific receptors, opsonin activities and plasma dysopsonins regulate the in vivo clearance of particulate materials from the circulation. Poloxamine-908 coating modulates particle clearance by effectively blocking opsonization but still allowing for dysopsonization.

Animals↗
PubMed1988

Host defence to bacterial infection in the neonate.

Host defence to bacterial infection is mainly determined by opsonins, i.e., IgG antibodies and complement, and phagocytic cells, which co-operate to remove bacterial invaders from host tissues. Various studies have clearly documented distinct defects in both arms of host defence in the newborn period. Chemotaxis, i.e., directed migration of polymorphonuclear leukocytes (PMN) is impaired in the neonate. Phagocytosis of bacteria by neonatal PMN is normal, but post-phagocytic events, particularly metabolic activation and bacterial killing are impaired, the latter defect apparently due to diminished generation of reactive oxygen species. Both classical and alternative pathway activity of complement are mildly diminished (50-80% of adult values) in the term newborn, but are more severely decreased in the premature infant (20-40% of adult values in 28 to 36 weeks prematures). Opsonic activity of transplacentally-derived IgG when compared to maternal IgG is strikingly deficient against staphylococci and group B streptococci (GBS), in the latter case depending on the GBS serotype. Since opsonization is a key process in antibacterial defence, it is speculated that these opsonic defects of IgG may be an essential determinant of the neonate's susceptibility to disease due to these bacteria.

Bacterial Infections↗
PubMed1987

Effect of opsonization on oxidative metabolism of plaice (Pleuronectes platessa L.) neutrophils.

The effect of serum opsonization on Vibrio alginolyticus (heat-killed)-stimulated chemiluminescence (CL) by plaice kidney- and peritoneal exudate-derived neutrophils was investigated. Peritoneal neutrophils only recognized heat-labile and kidney neutrophils only heat-stable opsonic activity in normal serum. Specific antibody did not show opsonic activity nor any synergism with the normal serum opsonins for either neutrophil population. Evidence was found for the production, by plaice neutrophils, of H2O2, O2-, OH. and two or more, as yet unidentified, reactive oxygen species (ROS).

Animals↗
PubMed2005

The opsonising activity of a pentraxin-like protein isolated from snapper (Pagrus auratus, Sparidae) serum.

In mammals the pentraxins, C-reactive protein (CRP) and serum amyloid P component (SAP) are important components of the immune response. Although pentraxins have been isolated from a number of fish species few studies detail their functional immunological role. In this paper we report the establishment of a flow cytometry based assay to measure the phagocytic activity of isolated snapper head kidney leukocytes (HKLs). This assay was then used to examine the ability of a pentraxin-like protein isolated from the serum of snapper (P. auratus) (Sn-PLP) to act as an opsonin. Incubation of snapper head kidney leukocytes (HKL) with FITC-labelled beads resulted in uptake of these particles by approximately 35% of HKLs. Incubation of beads with Sn-PLP enhanced phagocytosis by snapper HKLs in a dose-dependant manner. Enhanced phagocytosis could be inhibited by addition of a rabbit anti-Sn-PLP antibody suggesting that Sn-PLP may act as a ligand for a HKL cell surface receptor. This study provides further evidence toward a functional role for pentraxins in the host defence repertoire of fish.

Animals↗
PubMed2004

Oligomerisation and carbohydrate binding in an Atlantic salmon serum C-type lectin consistent with non-self recognition.

A C-type lectin was previously isolated from the blood of healthy Atlantic salmon (Salmo salar) and this salmon serum lectin (SSL) was found to opsonise bacteria. Selective binding to bacteria in vivo requires that the lectin be able to recognise a carbohydrate pattern on the bacterial surface distinguishable from that of the host. In order to investigate this selectivity in the lectin, a phage-display antibody was prepared and then used for detection of lectin by Western blotting. A carbohydrate binding-inhibition assay with Western blot detection of the lectin showed mannose to be the primary ligand and related sugars including glucose, N-acetylglucosamine and methyl alpha-D-mannopyranoside to be additional ligands of this lectin. The SSL in serum detected by Western blotting was shown to form a complex oligomer. These results show that the salmon serum lectin is oligomeric in blood and that it recognizes a broad spectrum of carbohydrates with optimal binding to mannose. The lectin might therefore be an ideal opsonin for multiple salmon pathogens with carbohydrate arrays on their surfaces. No similar lectins were identified in the sera of other fish by Western blotting using the phage-display antibody. Molecular analysis will be required in order to determine whether homologous lectins are expressed in related fish species. It is anticipated that similar lectins might have related pathogen recognition roles in divergent fish species.

Analysis of Variance↗
PubMed2005

Serum complement factor I decreases Staphylococcus aureus phagocytosis.

Complement-mediated opsonization of Staphylococcus aureus is a critical host defense in animal models. Specifically, C3b and CD35 play important roles in effective opsonophagocytosis of S. aureus. We have shown that complement control protein factor I mediates cleavage of the complement opsonin C3b bound to the S. aureus surface. In this study, we examined the physiologic relevance of this observation by determining whether factor I-mediated cleavage of S. aureus-bound C3b decreased phagocytosis of S. aureus by neutrophils. Compared with controls, anti-factor I antibody inhibited C3b-cleavage on the S. aureus surface by >83% (as measured by iC3b generation) and increased phagocytosis of S. aureus by >100%. Treatment of C3b-coated S. aureus with factor I increased generation of iC3b (75%), decreased the total amount of C3-fragments bound to the S. aureus surface (58%), and decreased the number of bacteria phagocytosed (40%). Testing specifically for C3-fragments shed from the S. aureus surface, we found that factor I increased shedding (43%). Notably, these factor I-mediated effects were of the same magnitude regardless of whether factor H, a known cofactor for factor I, was present. These findings indicate that S. aureus benefits from, and possibly manipulates, the normally host-protective activity of factor I cleavage of C3b, which results in bacterial escape from complement-mediated opsonophagocytosis. Because escaping opsonophagocytosis-mediated destruction is a necessary mechanism for bacterial survival resulting in human disease, preventing cleavage of C3b on the S. aureus surface, and thereby enhancing opsonophagocytosis, is a promising potential target for therapeutic intervention.

Antibodies, Blocking↗
PubMed2005

Anti-opsonic properties of staphylokinase.

Recently we described a novel bacteriophage-encoded pathogenicity island in Staphylococcus aureus that harbors a number of virulence factors that are all involved in the evasion of innate immunity. Here we describe a mechanism by which staphylokinase (SAK), frequently present on this pathogenicity island, interferes with innate immune defenses: SAK is anti-opsonic. By activating human plasminogen (PLG) into plasmin (PL) at the bacterial surface, it creates bacterium-bound serine protease activity that leads to degradation of two major opsonins: human immunoglobulin G (IgG) and human C3b. Incubation of opsonized bacteria with PLG and SAK resulted in removal of anti-staphylococcal IgGs and C3b from the bacterial surface. In phagocytosis assays this proved to be a very efficient mechanism to reduce the opsonic activity of human IgG and serum. The fact that SAK activates human PLG at the bacterial surface and removes IgG as well as C3b makes this protein a unique anti-opsonic molecule.

Complement C3b↗
PubMed2006

Ficolin-2 recognizes DNA and participates in the clearance of dying host cells.

Ficolin-2 is a serum opsonin, which has been shown to be a pattern recognition molecule in the lectin complement activation pathway. Because innate immune mechanisms are involved in maintaining tissue homeostasis we hypothesized that Ficolin-2 also participate in the clearance of dying host cells. We found that Ficolin-2 binds to late apoptotic cells, as well as to apoptotic bodies and necrotic cells, but not to early apoptotic cells. We demonstrated that Ficolin-2 binds DNA in a calcium dependent manner and that DNA inhibits the binding to late apoptotic and necrotic cells, suggesting that DNA on permeable dying cells is a plausible ligand. Reconstituting serum deficient of Ficolin-2, C1q and mannose-binding lectin with Ficolin-2 augmented deposition of complement C4 on necrotic cells. Opsonization leads to an enhanced attachment/uptake of necrotic cells by macrophages. In conclusion dying host cells expose ligands with the capacity of binding Ficolin-2, which in turn leads to increased attachment and engulfment. Binding of Ficolin-2 to DNA points at nucleic acid exposed by permeable late apoptotic and necrotic cells as one of the ligands for Ficolin-2. Ficolin-2 may therefore be a scavenger molecule participating in the removal of host cells and maintenance of tissue homeostasis.

Animals↗
PubMed2006

Yeast-binding C-type lectin with opsonic activity from conger eel (Conger myriaster) skin mucus.

A mannose-specific lectin with agglutination activity against a yeast, Saccharomyces serevisiae, was purified from conger eel (Conger myriaster) skin mucus. The lectin, named conCL-s, has a tetrameric structure consisting of two non-covalently associated dimers whose constituent monomers with a molecular mass of about 16,000 Da are linked by a disulphide bond. conCL-s is composed of 173 amino acid residues including a 24-residue signal peptide, and belongs to the C-type lectin family, which is typically characterized by binding to sugar in a Ca2+-dependent manner. Nevertheless, conCL-s showed Ca2+-independent activity in its yeast-binding. The gene expression of the lectin was widely detected in external and internal mucosal tissues, i.e., skin, gills, tongue, buccal cavity wall and esophagus. In these tissues, mRNA of conCL-s was exclusively distributed in club cells, which are one of the major components of the epidermis and mucosal epithelium in Anguilliforme species. conCL-s showed agglutination activity to a bacterium, Escherichia coli. Furthermore, attachment of the lectin to microspheres significantly enhanced their phagocytosis in conger eel macrophages. These findings suggest that conCL-s acts as an opsonin and plays an important role in the innate immunity on the body surface in conger eels.

Agglutination↗
PubMed2004

Multiplex opsonophagocytosis assay (MOPA): a useful tool for the monitoring of the 7-valent pneumococcal conjugate vaccine.

Pneumococcal conjugate vaccination is highly efficacious against invasive diseases in young children. Since host protection is mainly mediated by opsonin-dependent phagocytosis, the in vitro measurement of opsonophagocytic activity of the anti-capsular antibodies is assumed to be a reliable correlate of protection to monitor vaccine efficacy. Unfortunately, the methods used so far are all tedious to perform and material-consuming. Therefore, we modified the multi-specificity opsonophagocytosis killing assay (MSOPKA) into a high-throughput method, which simultaneously measures the opsonophagocytosis against the seven serotypes covered by the current conjugate vaccine in a single assay. In the so-called multiplex opsonophagocytosis assay (MOPA), a mixture containing equal numbers of colony forming units (CFUs) of chloramphenicol-resistant serotype 4, spectinomycin-resistant serotype 6B, streptomycin-resistant serotype 9V, erythromycin-resistant serotype 14, rifampicin-resistant serotype 18C, tetracycline-resistant serotype 19F, and trimethoprim-resistant serotype 23F pneumococci was used as a target mixture and incubated with serial dilutions of test serum. After opsonophagocytosis by differentiated HL-60 cells in the presence of complement, the samples were spotted onto different blood agar plates containing the seven selective antibiotics, respectively. Opsonophagocytosis was calculated as the highest serum dilution resulting in 90% or more reduction in CFUs. The data obtained by this assay correlated well with the data obtained by the MSOPKA. In conclusion, the MOPA simultaneously measures opsonophagocytosis capacity of serum against the capsular serotypes included in the 7-valent pneumococcal conjugate vaccine in a high-throughput fashion, requiring low volumes of patient sera.

Antibodies, Bacterial↗
PubMed2004

Effects of tumor-enhancing IgG2 on macrophage function.

Macrophages (M phi) play a significant role in allograft rejection. We investigated whether tumor-enhancing (te) IgG(2) acting as a cytophilic opsonin affects allograft destruction. Our results demonstrate that immune Tennessee Swiss (TS) (H-2(s)) mouse M phi destroyed greater numbers of target C3H(f)/He (H-2(k)) tumor cells than did nonimmune M phi. The percentage of (51)Cr release from labeled tumor cells induced by immune M phi was 39.10 + 3.24% compared to nonimmune M phi 28.0 + 3.87%, while te IgG suppressed cytotoxicity toward C3H(f)/He tumor cells of normal TS M phi as manifested by less isotope release (19.60 + 3.13%) than that produced by normal TS M phi with non-enhancing IgG(2) (39.90 + 5.8%). Rather than facilitating survival of allogeneic fibrosarcoma cells, te IgG(2) alloantibody potentiated their destruction by immune TS M phi (isotope release of 52.90 + 3.46%) compared with that produced by immune M phi alone (39.10 + 3.24%). Cytophilic te IgG(2) on TS M phi was demonstrated with either C3H(f)/He red cells or tumor cells. Electron micrographs of M phi revealed tumor cell ingestion and attachment of ferritin-labeled IgG(2) alloantibody on M phi and target tumor cells. In contrast to protection, te IgG(2) alloantibody facilitates macrophage-mediated allograft destruction.

Animals↗
PubMed1981

Protective efficacy of a modified immune serum globulin in experimental group B streptococcal infection.

In spite of aggressive antimicrobial therapy and extensive support measures, the mortality rate in early-onset group B streptococcal infection continues to be exceedingly high. In previous studies, we have demonstrated that passive immunotherapy with fresh whole blood containing opsonic antibody-improved survival in human neonates with group B disease. Transfusion of whole blood, plasma, or other blood products has a number of drawbacks, however. In the present study, we have evaluated immune serum globulin and a preparation of ISG modified for intravenous use for levels of type-specific antibody, opsonic activity, and protective efficacy against type Ia, II, and III group B streptococci. Type-specific antibody was detected in most of the preparations tested. In general, the level in MISG was less than that in the comparison ISG lot. Opsonic activity was also detected in these preparations against the more antibody-sensitive group B strains but was not present for opsonin resistant strains of type Ia, II, and III. Both ISG and MISG provided protection in neonatal rats infected with group B streptococci; in most cases MISG was more efficacious than the ISG from which it was made. These studies suggest that passive immunotherapy with MISG may be a valuable adjunct to current regimens used in the management of early-onset group B disease. This would be especially so if donors could be selected whose serum or plasma contained high levels of opsonic and protective activity against both antibody-sensitive and antibody-resistant group B strains.

Animals↗
PubMed1989

Association of low levels of mannan-binding protein with a common defect of opsonisation.

Failure to opsonise bakers' yeast (Saccharomyces cerevisiae) is a defect found in 5-7% of the general population. In this study, the presence of the defect was linked with low levels of mannan-binding protein (MBP), a calcium-dependent serum lectin. Purified MBP corrected the defect in a dose-dependent way in an in-vitro assay measuring the deposition of complement moieties on a mannan-coated surface. There was a highly significant correlation between the serum MBP level and the generation of C3b opsonins in a population of healthy blood donors. The median MBP level of ten children previously shown to have the functional opsonic defect was 4.9 micrograms/l (range 2.5-35.0 micrograms/l) compared with 143 micrograms/l (range 2.5-880 micrograms/l) for a paediatric control group.

Adolescent↗