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At least 271 records · Page 15Linked to original sources
PubMed2004

[The effect of opsonins on erythrocytes phagocytosis in the vitreous--laboratory research (Part A)].

PURPOSE: We performed experimental investigations in vitro into the opsonization of Rh-positive erythrocytes by IgG anti-RhD antibodies and phagocytosis of erythrocytes in the vitreous body. MATERIAL AND METHODS: The vitreous has been taken from the corpses of young people. Anti-RhD antibodies came from preparations 'Gamma anti-D 150'. 1% Erytrocyte suspension of ccDee phenotype has been applied. Phagocytosis assay was performed in the medium of the vitreous and in Hank's solution. RESULTS: Phagocytosis assay performed in the vitreous and in Hank's solution did not display statistically significant differences. CONCLUSIONS: The investigations in vitro presented here, proved that immunological reactions are really occurring in the vitreous body. They provide a base for the explanation of activity mechanism of anti-RhD antibodies injected intraoculary in cases of hemorrhages into vitreous body.

Adult↗
PubMed2004

[The effect of opsonins on erythrocytes' phagocytosis in the vitreous--clinical observations (Part B)].

PURPOSE: We demonstrate clinical material collected during several years, which illustrates the possibilities of immunotherapy in intravitreous hemorrhages. MATERIAL AND METHODS: Immunotherapy was applied in 172 persons, Rh-positive in 174 eyes with intravitreal hemorrhages of a various etiology. The therapy consisted of injecting preparations containing IgG anti RhD antibodies into the vitreous. RESULTS: Visual acuity improvement has been obtained in 77.6% of eyes. CONCLUSIONS: Summing up the effects of immunotherapy of hemorrhages into the vitreous body, it is necessary to stress the simplicity of performance of the procedure, its insignificant invasions and security resulting from the application of natural, human immunoglobulin.

Erythrocytes↗
PubMed1991

Immunization against serogroup B meningococci. Opsonin response in vaccinees as measured by chemiluminescence.

One hundred and thirteen healthy volunteers were immunized twice (six weeks apart) with four different doses (12.5, 25, 50 and 100 micrograms, measured as protein content) of an outer membrane vesicle vaccine from a serogroup B meningococcal strain (44/76, B:15:P1.16) complexed to serogroup C meningococcal polysaccharide and/or Al(OH)3 i.e. 12 different vaccines. Serum opsonic activity against the serogroup B strain was measured using a chemiluminescence method. A significant rise in serum opsonic activity was demonstrated in 84 volunteers (74%) six weeks after the first injection and in 97 (86%) six weeks after the second. All vaccinees with low preimmunization values (less than 25 mVs) experienced a significant increase in opsonic activity. A dose-related response was most evident for the vaccines containing adjuvant, and these vaccines were associated with a maximum response six weeks after the second injection, while the vaccines without Al(OH)3 induced a peak response six weeks after the first injection. The postimmunization opsonic activity was similar to that found in convalescent sera, indicating that the vaccines may protect against serogroup B meningococcal disease.

Adolescent↗
PubMed1989

An IgA monoclonal antibody directed against type III antigen on group B streptococci acts as an opsonin.

We have investigated the mechanisms by which a murine IgA mAb directed against the type III Ag (IgA anti-III mAb) of group B streptococci (GBS) protects neonatal rats from lethal infection with these organisms. Purified IgA anti-III mAb enhanced phagocytosis of type III GBS by rat peritoneal macrophages in vitro by fourfold compared with phagocytosis of buffer-treated GBS. In the absence of antibody, neonatal rat serum did not promote phagocytosis, but addition of neonatal rat serum to GBS opsonized with IgA anti-III led to a sevenfold increase in phagocytosis. Heat inactivation of C destroyed the ability of neonatal rat serum to enhance phagocytosis in the presence of IgA. C3 deposition was observed when GBS coated with IgA anti-III mAb were incubated in untreated neonatal rat serum or in serum treated with Mg/EGTA. This latter observation suggested that C3 deposition occurred through activation of the alternative pathway. The control IgA mAb MOPC 315 did not enhance GBS ingestion or C3 deposition on GBS. Depletion of C in vivo by using cobra venom factor abolished the protective effect of IgA anti-III mAb in the neonatal rat model. These data suggest that the ability of this IgA to activate C further enhances its opsonic activity and may be essential for its protective effect in vivo.

Animals↗
PubMed1986

The role of opsonins in vacuolar sealing and the ingestion of zymosan by human neutrophils.

After opsonization with whole human serum, with IgG antibody alone or with C3 fragments alone, the ingestion of zymosan particles by human neutrophils was found to correlate most closely with the efficiency of C3 fragment deposition on the zymosan surface. Selective opsonization of zymosan particles with IgG did not promote phagocytosis at all in suspension, but could promote ingestion after particle-cell contact was induced by centrifugation. In contrast, zymosan particles in suspension selectively opsonized by C3 fragments were ingested as efficiently as those opsonized with whole serum, and we suggest that C3 fragments provide the principal stimulus for phagocytosis of zymosan. The process of vacuolar sealing was not dependent on the state of opsonization of the particles and was significantly more efficient with unopsonized particles, indicating that formation of unsealed vacuoles is not due to a failure of the 'zipper' mechanism of sequential interaction of cell surface receptors and opsonic ligands.

Adult↗
PubMed1985

Resistance to phagocytosis by group A streptococci: failure of deposited complement opsonins to interact with cellular receptors.

The previous finding that phagocytosis-resistant M+ group A streptococci bear quantities of C3 which are sufficient for phagocytosis of their M- derivatives was investigated at two levels. It was first established that the C3 associated with M+ streptococci was not able to promote adherence to cells bearing the complement receptors CR1 and CR3 under conditions in which M- streptococci readily attached. The molecular form of C3 bound to M+ and M- streptococci was then defined by adding 125I-C3 to serum used for opsonization. C3 eluted from the bacteria by chaotropic and hydrolytic agents was analyzed by SDS-PAGE, and revealed that both cell types bound the opsonic forms of C3, C3b, and iC3b. Furthermore, approximately 80% of the C3b and iC3b associated with both cell types was covalently bound to a surface component, although most of the C3 bound to M+ streptococci was detergent-extractable, whereas greater than 50% of that bound to M- streptococci was not. These findings demonstrate that the M+ surface is interfering with the receptor binding of deposited C3b and iC3b, and that this contributes to resistance to phagocytosis by these organisms.

Complement Activation↗
PubMed1986

Pasteurella haemolytica leukotoxin: chemiluminescent responses of peripheral blood leukocytes from several different mammalian species to leukotoxin- and opsonin-treated living and killed Pasteurella haemolytica and Staphylococcus aureus.

A luminol-dependent chemiluminescence (LDCL) assay was used to assess the response of polymorphonuclear leukocyte (PMN) preparations from 4 species of ruminants (ie, cattle, sheep, goats, and antelopes) and 6 species of nonruminants (ie, swine, dogs, cats, rabbits, horses, and persons) to both opsonized and nonopsonized preparations of living and heat-killed Pasteurella haemolytica and Staphylococcus aureus and to opsonized and nonopsonized heat-killed strains of each bacterium in the presence of sterile culture supernatant (leukotoxin) from P haemolytica. The LDCL responses of PMN preparations from each of the species studied were greater for living than for heat-killed S aureus. The most efficient LDCL emission was observed with reaction mixtures containing opsonized living S aureus. Regardless whether they contained killed or living bacteria, the opsonized S aureus preparations elicited LDCL emissions more efficiently than did the corresponding nonopsonized preparations. Living P haemolytica cells and their sterile culture supernatant inhibited the LDCL emissions of phagocytically stimulated PMN preparations from ruminants, but not those from nonruminants. The LDCL response of ruminant PMN to nonopsonized living P haemolytica was characterized by the development of a peak response at 10 minutes of incubation followed by a precipitous decrease and a subsequent complete cessation of chemiluminescence. The peak LDCL response was higher for opsonized living P haemolytica than for nonopsonized living bacteria, and the increased response lasted longer. However, opsonization of living P haemolytica with the serum samples tested only temporarily spared the ruminant PMN preparations from the detrimental effects of leukotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗