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PubMed1993

A role for complement as the major opsonin in the sequestration of erythrocytes from elderly and young donors.

Erythrocytes from elderly donors (> 70 years), but not young donors (18-35 years), are shown to undergo sequestration in an in vitro erythrophagocytosis assay. Comparable levels of sequestration are observed for high density erythrocytes from young individuals and both low density and high density erythrocytes from elderly individuals. These cells, which are susceptible to phagocytosis with no additional treatment are collectively termed 'in situ aged' erythrocytes. We present evidence for the involvement of complement in the sequestration of 'in situ aged' erythrocytes and correlate levels of complement bound to 'in situ aged' erythrocytes from young and elderly donors with levels of phagocytosis. We also demonstrate that the in vitro sequestration of erythrocytes from elderly donors can be inhibited by beta-galactosyl sugars and arginine-glycine-aspartic acid (RGD) but not by mannose nor by Protein-G, a specific inhibitor of Fc-gamma mediated phagocytosis. These experiments show that IgG is not the major opsonin in the sequestration of red cells from elderly donors. In support of the role of complement rather than IgG as the major opsonin in red cell sequestration, we further demonstrate that C'3 bearing immune complexes block in vitro sequestration of erythrocytes from elderly donors. This competition is not dependent upon the isotype of the immunoglobulin (IgM or IgG) in the complex but rather on the presence of active complement.

Adolescent↗
PubMed1987

Standardization of a chemiluminescence method for the measurement of meningococcal opsonins using ethanol fixed meningococci.

A chemiluminescence (CL) method using polymorphonuclear leukocytes (PMNLs) and an automatic photoluminometer was used to measure serum opsonins to viable and inactivated group B meningococci. Continuous mixing at 37 degrees C both during opsonization and phagocytosis was essential for optimal CL responses. The CL response increased rapidly during an opsonization time up to 7.5 min, and with PMNL and bacteria concentrations up to 37.5 X 10(5) and 3.8 X 10(7) cells/ml, respectively. Opsonized ethanol fixed meningococci gave CL responses similar to those of viable meningococci, but had a better reproducibility. Using the ethanol fixed bacteria, the variation of PMNLs from different donors, the day-to-day variation, and the coefficient of variation of the CL responses, were all less than 10%. The opsonic activity of convalescent sera from 10 patients with meningococcal disease was markedly higher than that of sera obtained during the acute phase of the disease. Thus, this standardized CL assay using ethanol fixed bacteria is a highly reproducible and sensitive method for measuring serum opsonins to meningococci.

Ethanol↗
PubMed1968

Reticuloendothelial blockade: effect of puromycin on opsonin-dependent recovery.

Reticuloendothelial blockade induced by the administration of a gelatinized "reticuloendothelial test lipid emulsion" is due to a loss of opsonic activity in the plasma. Recovery from blockade, which is associated with restoration of plasma opsonins, was inhibited by the administration of puromycin. The effect of puromycin appears to be mediated by inhibition of opsonin formation rather than a puromycin-induced macrophage defect in phagocytosis.

Animals↗
PubMed1979

Immunological specificity of heat-stable opsonins in immune and nonimmune sera and their interaction with non-encapsulated and encapsulated strains of Staphylococcus aureus.

The in vitro interactions between strains of Staphylococcus aureus and human polymorphonuclear leukocytes in the presence of immune and nonimmune sera were studied. Evidence indicated that phagocytosis of encapsulated strains occurred in the presence of specific homologous antiserum, whereas non-encapsulated strains were readily phagocytized by polymorphonuclear leukocytes in the presence of both normal and immune sera. Immunological analyses demonstrated that normal serum opsonins, which reacted with the non-encapsulated strains, were specifically directed against exposed mucopeptide moieties of the organisms. Sera rich in antimucopeptide antibodies were obtained from rabbits immunized with heterologous bacteria such as Escherichia coli and group A-variant streptococci and were shown to be effective in opsonizing the non-encapsulated strains of S. aureus. Fresh clinical isolates of S. aureus were noticeably more resistant to the opsonizing effects of the antimucopeptide antibodies. Results were presented which suggest that the surface structures of these clinical isolates are more diverse than laboratory-propagated strains and that these antiphagocytic surface antigens may be significant factors in masking the opsonizing effects of the mucopeptide opsonins which are present in most sera.

Antibodies, Bacterial↗
PubMed1985

Trypanolytic activity, agglutinins, and opsonins in sera from animals refractory to Trypanosoma lewisi.

An examination of sera from a range of animals refractory to Trypanosoma lewisi showed that some contain trypanolytic activity and agglutinins for this trypanosome. Trypanolytic activity was demonstrated in bovine, sheep, and rabbit serum. These sera were shown to also contain agglutinins. The trypanolytic activity in all three sera was abolished by heat inactivation at 56 degrees C for 30 min. Studies with bovine serum showed that the lytic activity was totally inhibited by the addition of EDTA but was only partially inhibited by ethylene glycol-bis(beta-aminoethyl ether)-N,N-tetraacetic acid-Mg2+, suggesting the involvement of both classical and alternate pathways of complement activation. Serum from the natural host, the rat but not mouse serum, was capable of inhibiting the trypanolytic activity of bovine serum. The agglutinins in bovine serum were specific, since they could be adsorbed out with T. lewisi but not T. musculi. They fractionated on gel filtration in the position expected for 19S antibodies. By using opsonization measuring techniques, it was found that mouse serum lacked opsonins to T. lewisi, although opsonic activity was detectable in human serum. The absence of agglutinins, trypanolysins, and opsonins in mouse serum suggests that other factors prevent the infection of mice by T. lewisi. From these findings, it would appear that the inability of T. lewisi to infect a range of mammals, with the exception of mice, could be due to the presence of antibodies, the ability to activate complement through the alternative pathway, or both. The absence of these recognition factors and the ability to evade the effects of alternative pathway activation may be important factors in the ability of this parasite to establish infections in rats.

Animals↗
PubMed1990

Growth inhibition of Cryptococcus neoformans by cultured human monocytes: role of the capsule, opsonins, the culture surface, and cytokines.

Despite a presumed critical role of macrophages in the host response to cryptococcal infections, previous studies have failed to show growth inhibition of encapsulated Cryptococcus neoformans by human peripheral blood cultured monocyte-derived macrophages (MO-M phi). Here, we examined whether MO-M phi could be induced to inhibit growth of an encapsulated strain and an isogenic acapsular mutant strain of C. neoformans. MO-M phi were cultured in microwells, and inhibition was measured by comparing CFU at 0 and 24 h after fungal challenge. MO-M phi cultured on plastic surfaces failed to inhibit growth of the encapsulated strain, even in the presence of pooled human serum and/or anticapsular antibody. Moreover, the presence of anticapsular antibody significantly enhanced fungal growth. However, if MO-M phi were cultured on surfaces coated with fibronectin or poly-L-lysine (but not laminin or collagen) and yeast cells were opsonized with pooled human serum, then complete growth inhibition occurred. Preincubation with various concentrations of tumor necrosis factor, granulocyte macrophage colony-stimulating factor, 1,25-dihydroxycholecalciferol, or supernatants from C. neoformans-stimulated lymphocytes failed to activate macrophages for enhanced antifungal activity. The addition of gamma interferon resulted in a significant loss of growth inhibition. For the acapsular strain, complete growth inhibition was observed regardless of the choice of culture surface, opsonins, or cytokines. Fungicidal activity, as measured by a significant decrement in CFU compared with the initial inoculum, was not observed under any conditions tested. These data demonstrate that macrophages are capable of inhibiting cryptococcal growth but that this capacity is markedly influenced by the culture surface, opsonins, cytokines, and the fungal capsule.

Antibodies, Fungal↗
PubMed1992

Cross-reacting serum opsonins in patients with meningococcal disease.

We have examined the opsonic activity of sera from patients with Neisseria meningitidis (B:15:P1.16) infections against different meningococcal strains, using flow cytometry and luminol-enhanced chemiluminescence. A marked increase in the phagocytosis of ethanol-fixed meningococcal strains of different serogroups, serotypes, and serosubtypes was demonstrated in the presence of convalescence sera compared with acute sera. Convalescence sera also caused a significant increase of leukocyte oxidative metabolism during phagocytosis, as measured by luminol-enhanced chemiluminescence. The sera contained a broad range of opsonins cross-reacting with serogroup A, B, C, W-135, and Y meningococci of different serotypes and serosubtypes, indicating that the cross-reacting opsonins recognized surface epitopes other than those determined by current serotyping schemes.

Adolescent↗
PubMed2003

Mannose-binding lectin is a disease modifier in clinical malaria and may function as opsonin for Plasmodium falciparum-infected erythrocytes.

Variant alleles in the mannose-binding lectin (MBL) gene (mbl2) causing low levels of functional MBL are associated with susceptibility to different infections and are common in areas where malaria is endemic. Therefore, we investigated whether MBL variant alleles in 551 children from Ghana were associated with the occurrence and outcome parameters of Plasmodium falciparum malaria and asked whether MBL may function as an opsonin for P. falciparum. No difference in MBL genotype frequency was observed between infected and noninfected children or between children with cerebral malaria and/or severe malarial anemia and children with uncomplicated malaria. However, patients with complicated malaria who were homozygous for MBL variant alleles had significantly higher parasite counts and lower blood glucose levels than their MBL-competent counterparts. Distinct calcium-dependent binding of MBL to the membrane of P. falciparum-infected erythrocytes, which could be inhibited by mannose, was observed. Further characterization revealed that MBL reacted with a P. falciparum glycoprotein identical to the 78-kDa glucose-regulated stress protein of P. falciparum. MBL seems to be a disease modifier in clinical malaria and to function as an opsonin for erythrocytes invaded by P. falciparum and may thus be involved in sequestration of the parasite, which in turn may explain the association between homozygosity for MBL variant alleles and high parasite counts.

Adolescent↗
PubMed1990

Protracted enteric cryptosporidial infection in selective immunoglobulin A and saccharomyces opsonin deficiencies.

Chronic cryptosporidial infection in man usually occurs in those who are immunocompromised. We report a patient with a one year history of bowel symptoms resulting from persistent cryptosporidial infection of the colon. Investigations showed underlying selective IgA and saccharomyces opsonin deficiencies but no evidence of cell mediated immune dysfunction. Both selective immunoglobulin A and opsonin deficiencies are relatively common in the general population and may be a cause of susceptibility to persistent cryptosporidial infection.

Chronic Disease↗
PubMed1995

Differential release of superoxide anions by macrophages treated with long and short fibre amosite asbestos is a consequence of differential affinity for opsonin.

OBJECTIVE: To investigate the ability of short and long fibre samples of amosite asbestos to stimulate superoxide production in isolated rat alveolar macrophages, and to determine how opsonisation with rat immunoglobulin might modify this response. METHODS: Macrophages were isolated from rat lung by bronchoalveolar lavage and challenged with both opsonised and non-opsonised long and short fibres of amosite asbestos. Release of superoxide anions was measured by the spectrophotometric reduction of cytochrome c, in the presence and absence of superoxide dismutase. RESULTS: Both long and short fibre samples of amosite asbestos without opsonisation were ineffective in stimulating isolated rat alveolar macrophages to release superoxide anions in vitro. After opsonisation with immunoglobulin, however, a dramatic enhancement of release of superoxide anion was seen with long fibres, but not short, which confirms the importance of fibre length in mediating biological effects. The increased biological activity of the long fibre sample is explained by increased binding of the opsonin to the fibre surface as, at equal mass, the long fibres bound threefold more immunoglobulin than the short fibres. CONCLUSION: Opsonisation is an important factor in modulation of the biological activity of fibres at the cellular level. Differences in binding of opsonin to samples of fibre previously considered to be identical apart from length, suggest that surface reactivity needs to be taken into account when fibres are compared. Binding of biological molecules, in vivo, may thus be an important modifying factor in the pathological processes initiated by fibres.

Animals↗
PubMed2004

PTX3 function as an opsonin for the dectin-1-dependent internalization of zymosan by macrophages.

Pentraxin 3 (PTX3) is a tumor necrosis factor and interleukin-1beta-stimulated gene that encodes a long PTX with proinflammatory activity. Here, we show that peritoneal macrophages derived from PTX3 transgenic (Tg) mice express higher levels of PTX3 mRNA than macrophages from wild-type (WT) mice, at basal level as well as upon stimulation with zymosan (Zy). Macrophages from Tg mice also showed improved opsonin-independent phagocytosis of Zy particles and the yeast form of the fungus Paracoccidioides brasiliensis. In the case of P. brasiliensis, an enhanced microbicidal activity accompanied by higher production of nitric oxide was also observed in macrophages from Tg mice. Using fluorescein-activated cell sorter analysis and reverse transcriptase-polymerase chain reaction, we demonstrated that basal level of Toll-like receptor-6 and Zy-induced dectin-1 expression was slightly but consistently higher in macrophages from Tg mice than in macrophages from WT mice. Recombinant (r)PTX3 protein binds to Zy particles as well as to yeast cells of P. brasiliensis and addition of rPTX3, to a culture of WT-derived macrophages containing Zy leads to an increase in the phagocytic index, which parallels that of Tg-derived macrophages, demonstrating the opsonin-like activity of PTX3. It is important that blockade of dectin-1 receptor inhibited the phagocytosis of Zy particles by WT and PTX3 Tg macrophages, pointing out the relevant role of dectin-1 as the main receptor involved in Zy uptake. Our results provide evidence for a role of PTX3 as an important component of the innate-immune response and as part of the host mechanisms that control fungal recognition and phagocytosis.

Animals↗
PubMed2004

The sea urchin complement homologue, SpC3, functions as an opsonin.

The purple sea urchin Strongylocentrotus purpuratus expresses a homologue of complement component C3 (SpC3), which acts as a humoral opsonin. Significantly increased phagocytic activity was evident when yeast target cells were opsonized after incubation with coelomic fluid containing SpC3. SpC3 could be detected on the surface of yeast, and phagocytic activity could be inhibited by an anti-SpC3 antibody. This indicates that SpC3 promotes phagocytosis by physically tagging target cells for ingestion. Confocal microscopy showed that opsonized yeast were phagocytosed by a single coelomocyte type (polygonal phagocytes), presumably because these cells express SpC3 receptors. Overall, these data indicate that SpC3 is a major humoral opsonin in S. purpuratus coelomic fluid.

Animals↗
PubMed1991

Serum opsonins to serogroup B meningococci after disease and vaccination.

In this review the results of three previous studies are compared and discussed. Sera from 101 patients with meningococcal disease and from 113 volunteers immunized twice with vaccine preparations against serogroup B meningococci were examined for antimeningococcal opsonic activity using a chemiluminescence (CL) method. Twelve groups of vaccinees were immunized twice with one of four different doses of an outer membrane vesicle (OMV) preparation either alone or complexed to serogroup C polysaccharide and/or the adjuvant Al(OH)3. The OMV vaccine strain (44/76) was a patient isolate characterized as B:15:P1.16. The 89 surviving patients and 97/113 volunteers responded with significantly increased opsonic activity to the vaccine strain. Sera from all vaccinees with low preimmunization levels demonstrated a significant postimmunization increase in opsonic activity. The vaccine response was dose related, and the second injection induced a booster response in those who received preparations containing Al(OH)3. At 26 weeks a reduction in opsonic activity to preimmunization levels was noted in 19/97 previous responders. The reduction was less pronounced in those who were immunized with the higher doses. Using CL and flow cytometry we found vaccinee sera to show cross reacting opsonin responses to other serogroups and serotypes of meningococci except meningococci of serotype 2a and 2b. The increase in antimeningococcal opsonins after vaccination suggests that the serogroup B OMV vaccine may induce protection against clinical disease.

Adolescent↗
PubMed1990

Selective down-regulation of alveolar macrophage oxidative response to opsonin-independent phagocytosis.

We have compared the oxidative response of alveolar macrophages (AM) during opsonin-dependent and independent phagocytosis by using multiparameter flow cytometry. The respiratory burst of AM during phagocytosis was quantitated by the intracellular oxidation of the nonfluorescent precursors dichlorofluorescin diacetate (DCFH) or hydroethidine (HE, a reduced precursor of ethidium) to their fluorescent (oxidized) counterparts. After loading freshly isolated normal hamster AM with DCFH or HE, red or green fluorescent beads, respectively, were added to the shaking cell suspensions. Ingestion of opsonized particles by AM caused a marked increase in oxidation of both DCFH and HE proportional to the number of beads ingested. In contrast, uptake of one to three unopsonized particles per cell led to inhibition of oxidative activity compared to control cells incubated without particles. AM ingesting four or more unopsonized particles showed some increase in oxidative metabolism, but far less than that with identical numbers of particles in opsonin-dependent ingestion. Similar results were obtained using fluorescent labeled staphylococcal bacteria. Using three-color flow cytometry to study cells ingesting both types of particles, cells first ingesting unopsonized beads were also found to have an inhibited oxidative response to subsequently ingested opsonized particles. The mitochondrial poison antimycin inhibited most of the intracellular oxidative response to either type of phagocytosis. The remaining antimycin-insensitive, membrane derived respiratory burst of AM was also substantially diminished after phagocytosis of unopsonized particles vs similar numbers of opsonized particles. The greatly increased mitochondrial respiration in AM during phagocytosis of opsonized particles may be related to bactericidal mechanisms. Killing of ingested Staphylococcus by AM was markedly impaired in the presence of antimycin. The results suggest that AM may ingest the numerous, unopsonized inert particles that are inhaled without generation of potentially toxic oxygen metabolites, while retaining the capacity to undergo a respiratory burst after ingesting opsonized particles and bacteria. The mechanism(s) for this distinct response may include generation of an inhibitor of intracellular oxidative metabolism.

Animals↗
PubMed1984

Murine anti-lymphocyte monoclonal antibodies fail to act as opsonins for allogeneic human peripheral blood polymorphonuclear phagocytes.

Seven murine monoclonal antibodies (MoAbs) to antigenic determinants present on human lymphocytes did not promote phagocytosis of allogeneic human lymphocytes by human peripheral blood polymorphonuclear leucocytes (PML). Similarly there was no significant metabolic activation of PML as determined by incorporation of radiolabelled iodide. The opsonic activity of MoAbs was not enhanced by addition of human or rabbit complement nor by the use of sheep anti-mouse IgG, rabbit anti-mouse immunoglobulin or goat anti-mouse immunoglobulin as second antibody. Whole serum from mice immunized with human lymphocytes did not act as an opsonin when tested with human PML. Hyperimmune mouse antiserum to Bordetella pertussis antigen acted only weakly as an opsonin. Human PML may not have an in vivo role in the removal of allogeneic lymphocytes treated with murine anti-lymphocyte MoAbs.

Animals↗
PubMed1984

Opsonins in normal mouse serum for the phagocytic killing of Proteus mirabilis by murine neutrophils.

An assay of phagocytic killing by murine neutrophils in homologous serum was used to determine the nature of the opsonins in normal mouse serum for phagocytic killing of Proteus mirabilis. Leucocytes from the peritoneal cavities of mice given an intraperitoneal inoculation of brain-heart infusion broth 3 h previously, phagocytosed and killed P. mirabilis in a 2-h assay in the presence of 10% serum from normal mice. The serum factors supporting phagocytic killing were heat-labile (50 degrees C or 56 degrees C for 30 min) and could be absorbed at 37 degrees C but not 4 degrees C by three different species of Gram-negative bacteria. The tested species of Gram-positive bacterium did not absorb the activity. At the end of the assays, greater than 90% of leucocyte-associated bacteria were associated with neutrophils. Leucocytes from unstimulated peritoneal cavities (less than I% neutrophils) did not kill bacteria in this assay, in contrast to leucocyte suspensions containing up to 98% neutrophils. These findings indicated that the phagocytic killing of P. mirabilis in this assay was mediated by neutrophils, and that complement fixation by the alternative pathway provided necessary opsonins in normal mouse serum.

Animals↗
PubMed1983

The effect of C3 levels on yeast opsonization by normal and pathological sera: identification of a complement independent opsonin.

The ability of 150 normal and pathological sera to opsonize yeast for uptake by isolated human polymorphonuclear leucocytes has been studied. Phagocytosis was measured by an assay depending on electronic particle counting to measure yeast uptake and by a new fluorometric assay which is able to distinguish particle adherence from true phagocytosis. The opsonic activity of normal human serum was heat labile and depended markedly on C3 levels. The sera of 6% of healthy young adults (three from 45) and 8% of healthy donors aged 65-88 (four from 57) showed defective opsonization in spite of normal C3 and CH50 levels. Thirty-eight pathological sera with low C3 levels showed defective opsonization. However, three sera with low C3 levels showed apparently normal opsonic activity. The opsonin from two of these sera was characterized. It was heat stable, had apparent mol.wt of 400,000 and was active in serum free media. The opsonin was absorbed by immobilized Staphylococcus aureus and by gelatin-Sepharose, suggesting that it is related to fibronectin. Fibronectin from normal human sera prepared by affinity chromatography on gelatin-Sepharose was not opsonic in this system.

Adult↗
PubMed1995

Increased opsonization of a prtH-defective mutant of Porphyromonas gingivalis W83 is caused by reduced degradation of complement-derived opsonins.

Periodontitis is a disease of the supporting structures of the teeth that is caused by bacteria whose common ecologic niche is the gingival crevice or the periodontal pocket. Tissue destruction occurs in spite of both local and systemic immune responses against such bacteria. Porphyromonas gingivalis is considered to be an important pathogen in some forms of human periodontitis and is particularly interesting because of its multiplicity of virulence factors. We have previously observed that phagocytosis-resistant invasive strains of P. gingivalis proteolytically degrade C3 and IgG and accumulate less C3-derived opsonins during complement activation. We recently have cloned the prtH gene from P. gingivalis W83 that encodes a 97-kDa active protease, which has the capacity to degrade purified C3 protein. By using this cloned gene we created an allelic exchange mutant of P. gingivalis W83, designated V2296, in which the prtH gene was inactivated. This mutant was previously shown to be less virulent than its parent strain W83 in a mouse model of bacterial invasiveness. In the present study we have assessed the relative capacity of V2296 and W83 to be opsonized by complement and to be taken up by PMNs. The data demonstrate that V2296, in comparison with its parent strain W83, is less able to degrade C3 and that it accumulates significantly greater numbers of molecules of C3-derived opsonins on the bacterial surface in the form of C3b and iC3b during complement activation. Furthermore, opsonized V2296 is taken up in much higher numbers by human PMNs than W83, suggesting that the prtH gene product may be important in evasion of host defense mechanisms.

Antigens, Bacterial↗