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PubMed1990

Deficiencies in opsonic defense to pneumococci in the human newborn despite adequate levels of complement and specific IgG antibodies.

We studied the major determinants of opsonophagocytosis against Streptococcus pneumoniae serotypes 14 and 19 in paired cord/maternal sera from 27 healthy term and 24 preterm infants in an attempt to gain more insight in the susceptibility of newborns to pneumococcal infection. For both pneumococcal serotypes studied, opsonic activity in neonatal sera varied greatly, but was moderately to profoundly deficient when compared to paired maternal sera, both in preterm (34.5 and 34.9% of the activity in maternal serum, for serotypes 14 and 19, respectively, p less than 0.001 for both) and in term serum (43.5 and 52.7% of the activity in maternal serum, for serotypes 14 and 19, respectively, p less than 0.001 for both). The opsonic deficiency in preterm sera could be ascribed to a diminished level of the major opsonins for pneumococci, i.e. complement factor C3 deposited on the bacterial surface (69.5 and 66.2% of C3 deposition in maternal serum on serotypes 14 and 19, respectively, p less than 0.01 for both) and specific anticapsular IgG antibodies (48.5 and 14.1% of maternal levels for serotypes 14 and 19, respectively, p less than 0.001 for both). However, the opsonic defect in serum from term infants could not be explained in a similar way, because C3 deposition and specific anticapsular IgG levels were equal to the values found in the paired maternal sera. Therefore, we conclude that the opsonic defect in newborn serum for pneumococci cannot be solely explained by a deficiency in the major opsonins for these bacteria. A dysfunction in these opsonins seems to be a more likely explanation for the observed opsonic defect in the neonate.

Antibodies, Bacterial↗

PubMed1975

Serum factors capable of opsonizing Shigella for phagocytosis by polymorphonuclear neutrophils.

Twenty-five Shigella strains were tested for their susceptibility to phagocytosis and killing by polymorphonuclear neutrophils (PMN). The studies identified several serum factors that could participate in opsonization. The strains varied remarkably in their susceptibility to killing when heat-stable opsonins were employed, but all strains were killed when exposed to heat-labile opsonins and PMN. The heat-stable opsonin was shown to be IgG, whereas IgM was ineffective in the absence of complement, and 11S IgA was never effective. Heat labile opsonization required immunoglobulin as well as complement, but IgM was the only immunoglobulin demonstrated to participate in this reaction. The alternative C3 activating pathway is required for efficient heat-labile opsonization of Shigella, but some opsonization also appeared to occur through the C1-C4-C2 pathway of C3 activation.

Antibodies, Bacterial↗

PubMed1989

[Therapeutic implication of plasma C3 rich fraction against bacterial infection in surgical patients].

The depleted plasma opsonic activity is a major provoking cause of severe postoperative infection in patients who underwent extended surgical procedures. In order to establish the therapeutic use of C3 rich fraction (C3RF) for these patients in place of large amount of fresh frozen plasma (FFP) replacement, a basic study was done dealt with this fraction which was extracted from FFP with polyethyleneglycol. The results were as follows. (1) Addition of minimum amount of C3RF in vitro sufficiently revived the opsonic activity of opsonin exhausted guinea pig's plasma with heating or treating with cobra venom factor (CVF). (2) The clearance of E. coli 075 from peritoneal cavity and from blood stream in CVF treated guinea pigs was much delayed. However, in vivo administration of C3RF remarkably improved the clearance of bacteria and survival rate of opsonin depleted animal in E. coli peritonitis (p less than 0.05). (3) Opsonin lowered plasma samples in postoperative, septic, or cirrhotic patients were revived by not only replacing FFP, but also by adding minimum amount of C3RF. These results suggest that transfusion of C3RF should have beneficial effect in surgical patients with severely depleted plasma opsonic activity.

Aged↗

PubMed1985

A rapid and simple method for evaluation of serum opsonic capacity against Bordetella pertussis by chemiluminescence.

Serum opsonic capacity against Bordetella pertussis was studied by using quantitative chemiluminescence (CL) which is known to have several advantages over conventional methods in the evaluation of opsonization and phagocytosis. For opsonization, sera from whooping cough patients or from controls were incubated with killed B. pertussis cells at 37 degrees C for 30 min. Polymorphonuclear leukocytes, mononuclear cells or unfractionated leukocytes, all from healthy blood donors, were added to the opsonization mixture and CL emission was measured. Bacteria opsonized in diluted sera of whooping cough patients caused the activation of leukocytes manifested as a CL emission and no CL emission was observed when unopsonized B. pertussis was incubated with leukocytes. The opsonins could be detected by using any type of leukocyte preparation. Sera from adults vaccinated with DTP in the childhood gave rise to a large CL emission. Sera from whooping cough patients produced CL responses in more dilute solutions than those from vaccinated controls and sera from unvaccinated infants did not contain opsonins against B. pertussis. In unvaccinated infants suffering from whooping cough no opsonins were detectable in sera collected one week after the onset of the disease. However, the development of the opsonic capability against B. pertussis was observed in follow-up sera of all patients. The CL assay is simple, rapid, and reproducible offering new possibilities to evaluate humoral immune mechanisms and phagocytosis in whooping cough.

Adult↗

PubMed1982

A role for IgM in the in vitro opsonisation of Staphylococcus aureus and Escherichia coli by bovine polymorphonuclear leucocytes.

The phagocytosis and killing of Escherichia coli (strain P4) and Staphylococcus aureus (strain M60) by bovine polymorphonuclear lymphocytes (PMN) suspended in phosphate buffered saline, requires the presence of calcium ions and opsonins. The highest dilution of normal decomplemented adult sera in which the opsonins are still active is approximately 1/1000 for S aureus and 1/200 for E coli. In fetal and precolostral sera heat labile factors are also required for opsonising E coli but these are not required for S aureus. IgG1 and IgG2 from adult sera did not opsonise the bacteria even though receptors for IgG2 anti-erythrocyte antibodies have been reported on bovine and ovine PMN. A systematic separation of adult serum proteins was carried out by salt fractionation, anion exchange and gel filtration chromatography. The results suggest strongly that the opsonin in adult bovine sera is IgM.

Animals↗

PubMed1987

A rapid fluorescent assay to distinguish attached from phagocytized yeast particles.

In studies of phagocytosis and its consequences for cell activation, it is important to distinguish those particulate stimuli which are completely ingested and internalized from those which are only attached to phagocytic surfaces. Ingestion can be profoundly influenced by both the type of opsonins on the surface of the stimulus and the expression and activation of receptors on the phagocytes for these opsonins. We report a new fluorescent assay which facilitates rapid and reproducible quantitation of attached versus fully internalized live or dead yeast particles by phagocytes. The assay employs the fluorescent dye diaethanol (Uvitex 2B) which stains chitin on the cell wall of fungi and is excluded from live phagocytes. The diaethanol assay and a standard, previously published methylene blue dye exclusion assay yielded comparable results using human neutrophils or monocytes incubated with heat-killed, serum-opsonized Candida albicans. The diaethanol assay proved useful in distinguishing differences in effects of various opsonins, as human neutrophils selectively opsonized with either pooled human serum (PHS), IgG (heat-inactivated PHS) or complement (IgG-depleted PHS) completely internalized 69.5%, 91.3% and 52.5% of cell-associated zymosan particles respectively. Finally, the new assay permitted comparisons of differing macrophage populations, as resident murine peritoneal macrophages internalized only 10.6% of complement-opsonized, cell-associated zymosan particles compared with 41.7% when the macrophages were elicited with thioglycolate. The assay should prove useful to investigators studying both fungal phagocytosis and killing, as well as to those performing general studies of receptor expression, regulation and function.

Candida albicans↗

PubMed1984

The effects of malnutrition on serum fibronectin and reticuloendothelial function.

A rat model was used to investigate the effects of starvation and protein depletion on serum fibronectin levels and reticuloendothelial function. Serum fibronectin levels decreased significantly following both test diets. The uptake of opsonin-independent test agents was minimally affected by starvation and protein depletion. Clearance of gelatinized colloidal carbon, which is dependent on circulating opsonins, was significantly reduced in the malnourished animals. This clearance defect was corrected by incubation of colloidal carbon with normal serum. These data suggest that reticuloendothelial dysfunction secondary to malnutrition is primarily mediated by a deficiency of circulating opsonins.

Albumins↗

PubMed1998

Impaired phagocyte oxidative capacity in patients with human immunodeficiency virus infection.

Bacterial infections that may be related to impaired phagocyte function often develop in patients infected with human immunodeficiency virus (HIV). We examined the oxidative capacity of circulating phagocytes in 78 HIV+ patients and 31 control subjects by measuring chemiluminescence with a whole blood assay. Phagocytes were stimulated with zymosan opsonized with human complement (hC-OPZ) or immunoglobulin (hI-OPZ) with or without exogenous primers. Patients with CD4+ < 500/microL showed reduced whole blood chemiluminescence at maximal opsonin receptor (MOR) activity after priming in response to hC-OPZ relative to control subjects, and the difference was significant for patients with CD4+ < 100/microL. Patients had lower absolute phagocyte counts; however, the chemiluminescence activity calculated per phagocyte count was significantly depressed in advanced HIV infection, indicating the impairment of phagocytic cell function and a reduction in number. Data were similar when hI-OPZ was used as a stimulus. The chemiluminescence of unprimed phagocytes at circulating opsonin receptor (COR) activity relative to maximally primed phagocytes (COR/MOR ratio) was significantly higher for HIV+ patients as compared with control subjects and indicates a defect in phagocyte priming. Alternatively, the phagocytes do not increase chemiluminescence with priming because they have already been primed or activated in vivo. In late-stage disease, decreased opsonin receptor-dependent respiratory burst activity contributes to the risk of secondary bacterial infections.

Adult↗

PubMed2002

Important role of serum proteins associated on the surface of particles in their hepatic disposition.

To elucidate the important factors for the difference in the hepatic disposition between polystyrene nanospheres with a size of 50 nm (NS-50) and lecithin-coated NS-50 (LNS-50), the liver perfusion studies and the in vitro uptake studies using the cultured Kupffer cells were performed. It was suggested that opsonin-mediated phagocytosis is not significantly involved in the hepatic disposition of LNS-50 in the presence of serum, whereas its involvement in the hepatic uptake of NS-50 was clearly demonstrated. Western blot analysis showed that IgG, complement C3, and fibronectin, well-known opsonins in the serum, adsorbed on the surface of NS-50 in larger amount than on the surface of LNS-50. On the other hand, serum albumin, which was suggested to function as a dysopsonin for the hepatic disposition of NS-50, was associated with both spheres almost to the same extent. These findings suggest that the hepatic disposition of LNS-50 at lower level should be ascribed to the less amount of serum opsonins associated on the surface and that the serum proteins associated with these spheres should be important as a determinant for their hepatic disposition.

Animals↗

PubMed2000

Opsonic function and concentration of human serum ficolin/P35.

Collectins, C-type (Ca2+-dependent) animal lectins with both collagenous and carbohydrate recognition domains, function as opsonins against pathogens. We previously described an N-acetylglucosamine (GlcNAc)-binding lectin (ficolin/P35) with a collagen- and a fibrinogen-like sequence present in human serum. In this report we show that ficolin/P35 can serve as an opsonin and enhance the clearance of pathogens having surface GlcNAc. Ficolin/P35 bound to an Ra chemotype strain of Salmonella typhimurium (TV119) which has an exposed GlcNAc at the non-reducing termini of the polysaccharide. On the other hand, ficolin/P35 did not bind to LT2, a smooth type strain of S. typhimurium with additional O-polysaccharides covering GlcNAc. Ficolin/P35 enhanced the uptake of TV119 by monocytes or polymorphonuclear leukocytes but had no opsonic activity towards LT2. These results suggest that, like collectins, ficolin/P35 is a collagenous lectin which has a role in innate immunity against certain pathogenic organisms by acting as an opsonin. We prepared monoclonal antibodies against ficolin/P35 and developed an enzyme-linked immunosorbent assay (ELISA) for measuring ficolin/P35 concentrations in humans. The mean serum concentration of ficolin/P35 from 130 normal individuals was estimated to be 13.7 microg/ml.

Carrier Proteins↗

PubMed1985

Phagocytic defense in the lung.

Phagocytic defense in the normal lung is shared principally by two kinds of cells - alveolar macrophages that reside on the air surface and roam the alveoli and PMNs that circulate in the intravascular space or are stored transiently in areas adjacent to the capillary-alveolar interface (marginated in capillaries) and can reach the alveolar space quickly. The nature of the stimulating microorganism or aerosol particle reaching the alveolar surface may determine which phagocytic cell ultimately responds to contain the intruder. Ingestion and containment (either intracellular killing or enzymatic degradation) are the goals, and an 'opsonin' may be necessary to enhance the efficiency of phagocytosis. In the lung this is very complex, reflecting the interdependence on immune and nonimmune opsonins. For immune mediated phagocytosis by alveolar macrophages, IgG antibody is preferable. Among the four subclasses of IgG, certain ones seem to bind preferentially to macrophages, whereas others are already adherent to the cells as cytophilic antibody. In the respiratory tract milieu of subjects with CF, the interaction of immune and nonimmune opsonins is much more complex because of proteolytic enzymes that can degrade antibodies creating various fragments. Now that we are in an era of very specific humoral replacement therapy with intravenous IgG that contains IgG subclasses and the potential for using monoclonal antibodies for very precisely directed replacement, special attention must be given to identifying the appropriate class and subclass of antibody that may be required. This may be relatively simple when forms of passive immune therapy are being considered. More difficult will be devising ways to actively immunize patients (or animals) and manipulate their antibody responses so that selective immunoglobulin subclasses are produced. To obtain such control over the humoral immune response will require much more basic work in animal models. More attention to the form of immunizing antigen, type of adjuvant and site of administration will be required. Finally, selective immunization of the mucosal surfaces of the airways will present different challenges than parenteral methods that elicit systemic responses and may not be satisfactory to prevent certain respiratory infections. The prospects are exciting despite much work in cellular immunology that remains for the future.

Animals↗

PubMed1975

Hepatic reticuloendothelial host defense failure following surgical trauma.

We evaluated potential pituitary-adrenal influences on postoperative reticuloendothelial (RE) function. Male dogs, 13 to 18 kg (28.6 to 39.6 lb), were used and the operative procedure was hemicolectomy. The RE function was evaluated by a colloid clearance technique and circulating opsonin levels were quantified by bioassay. Normal animals manifested RE depression three hours following incision (49 percent decline in the global phagocytic index K and an associated 30 percent decline in the circulating opsonic activity). Dexamethasone sodium phosphate pretreatment over a three-day preoperative period prevented the postoperative RE clearance failure (control K = 0.69; postoperative k = 0.79) however, a slight (18 percent) but not significant decrease in opsonic activity occurred. Cortisone acetate or adrenocorticotropic hormone over a wide-dosage range manifested no depressing effect on in vitro phagocytosis. These studies, in conjunction with our previous findings of Kupffer cell activation following adrenalectomy, as well as the demonstration of opsonin depletion and RE phagocytic depression following surgery in the absence of the adrenal glands suggest that the pituitary-adrenal system modulates postoperative RE phagocytosis.

Animals↗

PubMed1986

Opsonic dysfunction secondary to plasma fibronectin depletion after aortic surgery.

Fibronectin is a plasma opsonin which is depleted after major injury or surgery. The effect of major aortic surgery on plasma fibronectin has been studied in patients and in an equivalent experimental model in pigs. On the day after aortic surgery in eleven patients mean fibronectin (+/- s.e.m.) had fallen from 363 +/- 11 mg/l pre-operatively to 179 +/- 19 mg/l (P less than 0.01). No such fall was observed in patients undergoing herniorrhaphy. In fourteen pigs aortic surgery produced reproducible surgical shock and a fall in plasma fibronectin from 331 +/- 10 mg/l to 43 +/- 13 mg/l after resuscitation (P less than 0.01). Whenever plasma fibronectin fell below 190 mg/l the circulating free fibronectin was consumed in complexes of 1000 kDa containing collagenous debris. More severe depletion of plasma fibronectin was related to higher concentrations of circulating nonopsonized collagenous debris and to subsequent mortality in pigs. The depletion of free fibronectin that occurs following major surgery may produce clinically important opsonic dysfunction. The clinical relevance of this fibronectin consumption may be missed if measurement is limited to circulating fibronectin levels without determining that proportion bound in complexes and no longer available as an opsonin.

Animals↗

PubMed1985

Fibronectin assays and their clinical application: a review.

Cold insoluble globulin (fibronectin) was discovered 30 years ago but recently there has been a remarkable growth of knowledge concerning its interaction with the cell cytoskeleton and its role in cell-cell and cell-matrix adhesion. The protein is also a major plasma opsonin with a role in regulating fixed macrophage activity and it is this area in which clinical applications are now beginning to develop. Methods are discussed for measuring the concentration of the protein and its opsonic function in vitro, and for the evaluation of fixed macrophage function in vivo. Also discussed are the metabolism of the protein, the implications of opsonin depletion in patients with serious injury or infection and the attempts to reverse this with plasma protein replacement therapy.

Animals↗

PubMed1984

Interaction of plasma fibronectin (pFN) with membranous constituents of peritoneal exudate cells and pulmonary macrophages.

The prominent role of plasma fibronectin (pFN) in the host defense system as an opsonin for gelatin (collagen)-coated colloids has been established. In the present study we investigated the interaction of pFN and membrane isolates from cells devoid of collagen, as well as several tissues. In a liver slice assay system it was shown that subcellular membrane fractions from lung macrophages, peritoneal exudate cells, spleen, tests, and liver were able to competitively inhibit the pFN-mediated uptake of 125I-gelatin coated latex beads (gLtx) at low concentrations. Endocytosis of 125I-labeled membrane isolates by macrophage monolayers was also promoted by addition of pFN. In an attempt to characterize the membrane component(s) interacting with pFN, it was found that mild extraction procedure with 1 M KBr could release a significant amount of this inhibitory activity. Further studies demonstrated that the agent(s) responsible for inhibition of gLtx uptake was heat sensitive, not altered by trypsin treatment, and did not contain actin, a protein known to interact with pFN. This work indicates that pFN interacts specifically with an as yet unknown membrane component(s) and that such interaction will promote clearance of cellular debris by macrophages. This suggests that pFN may be an important opsonin for the reticuloendothelial system in clearance of collagenous and noncollagenous cellular debris once they are exposed to interact with it.

Animals↗

PubMed1989

Lectin-mediated, nonopsonic phagocytosis of type 1 Escherichia coli by human peritoneal macrophages of uremic patients treated by peritoneal dialysis.

Human peritoneal macrophages isolated from uremic patients undergoing peritoneal dialysis bind type 1 fimbriated Escherichia coli in the absence of opsonins. The number of bacteria bound per macrophage was 6.9, as determined by microscopic examination. Methyl alpha-mannoside (0.1 mM) and p-nitrophenyl alpha-mannoside (0.01 mM) inhibited this binding by about 66%. The ability of peritoneal macrophages to bind E. coli in a mannose-specific manner was confirmed in further experiments using an enzyme-linked immunosorbent assay (ELISA) with an antibacterial antibody, radiolabelled E. coli, and counts of colony-forming units (CFU). The number of bacteria bound per macrophage was 7 to 12 in the ELISA and 5.5-8.5 in the CFU assay. Methyl alpha-mannoside caused 70% inhibition of binding in the ELISA and 84% in the CFU assay, whereas p-nitrophenyl alpha-mannoside showed inhibition of 79% and 90%, respectively. Most bound bacteria (76-80%) were subsequently killed. Nonfimbriated E. coli 827 bound poorly to the macrophages (approximately 22%) as compared to that of the fimbriated bacteria. Although this binding was not inhibited by methyl alpha-D-mannoside or p-nitrophenyl alpha-mannoside, the percentage of bacteria killed was similar to that of the fimbriated phenotype. The peritoneal macrophage is thus able to phagocytose E. coli in the absence of opsonins. This may explain the relative rarity of E. coli as an etiologic agent of peritoneal infections in the dialysed patient.

Adult↗

PubMedDate not supplied

Imaging the spatial distribution of membrane receptors during neutrophil phagocytosis.

Optical microscopy and image processing have been employed to study the distribution of several cell surface receptors on living human neutrophils during opsonin-dependent and opsonin-independent phagocytosis. Receptors were labeled using fluorescein-, rhodamine-, or AMCA-conjugated F(ab')2 fragments of anti-Fc gamma RIIIB (CD16), anti-CR3 (CD11b/CD18), and anti-uPAR (urokinase-type plasminogen activator receptor) antibodies, intact phycoerythrin-labeled interleukin 8, and fluorescein- or rhodamine-labeled Con A (concanavalin A), Boc-PLPLP (tert-butyl-oxycarbonyl-Phe(D)-Leu-Phe(D)-Leu-Phe-OH), and N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys. Labeled neutrophils were observed during the phagocytosis of IgG-opsonized erythrocytes and nonopsonized latex beads, Escherichia coli, and Staphylococcus aureus. To quantitate receptor distribution, cells were divided into four quadrants with the first being the point of attachment and the fourth being opposite the point of attachment. Ligated formyl peptide receptors, and to a lesser extent CR3, accumulated at the sites of target internalization for all forms of phagocytosis examined. However, Fc gamma RIIIB, uPAR, IL-8, Con A, and the FPR antagonist FBoc-PLPLP were not polarized on cells during phagocytosis. These data suggest that agonist-labeled formyl peptide receptors may play a broader role in leukocyte function than previously suggested, including possible participation in phagocytosis.

Amino Acid Sequence↗

PubMed1976

Latex phagocytosis by polymorphonuclear leukocytes. In vitro and in vivo studies with a simple screening test.

A simple semiquantitative slide test to assess the phagocytic activity of periphera polymorphonuclear leukocytes is described. Leukocytes are isolated from one drop of blood and latex particles are offered for phagocytosis. Cellular capacities and serum opsonins can be assessed separately. In the presence of pooled adult serum no defect of phagocytosis was seen in preterm and full-term newborns nor in pediatric patients with infectious or other diseases. In 4 of 7 premature newborns a definite deficiency of serum opsonins was demonstrated. In in vitro studies complement (plus possibly other heat-labile factors) promoted phagocytosis. Phagocytic rates were depressed by endotoxin and phenylbutazone.

Adult↗