Biomedical subjects

G Fóris

Publications and source records attributed to G Fóris.

At least 55 records · Page 3Linked to original sources

PubMed1983

Effect of low-molecular-weight lymphokine components on the Fc and C3b receptor-mediated macrophage functions.

Rat lymphokine (LK) components of 500--2500 MW separated on Sephadex G-15 column (FrA) were tested for their effect on Fc and C3b receptor activities of rat resident (rPM) and thioglycollate-provoked (pPM) peritoneal macrophages. Functions of the receptors were studied by measuring the adherence and uptake of 51Cr-labeled sheep red blood cells (SRBC) mediated by isolated rat anti-SRBC IgM or IgG2a antibodies and human C3, respectively. On rPMs mainly Fc mu receptors (Fc mu Rs) were affected by FrA; at low concentration (20 micrograms/ml) adherence was increased and phagocytosis was inhibited. At higher concentrations (40-80 micrograms/ml) a reverse effect was observed: adherence was inhibited and phagocytosis increased. On pPMs IgG2a-mediated functions were mainly affected by FrA with a concentration dependence like that observed with Fc mu Rs on rPM monolayers. A concentration-dependent enhancement of C3b receptor (C3bR)-mediated adherence by FrA was observed on both PM types. On pPms C3bR-mediated phagocytosis was enhanced as well.

Animals↗

PubMed1983

The effect of oligopeptides on the C3b receptor-mediated functions of rat macrophages.

Effects of various substances known to influence macrophage functions on the adherence of C3b-coated sheep erythrocytes (E-C3b) and their phagocytosis by elicited rat peritoneal macrophages (PM) has been studied. Different oligopeptides (OP) having a chemotactic effect, such as tuftsin, angiotensin II (At II) and the OP-fraction of a lymphokine preparation (LK-OP) increased both adherence and phagocytosis of E-C3b in a concentration-dependent fashion. In contrast, neither substances influencing the membrane cation transport nor prostaglandins (PG) and cyclic nucleotides significantly changed the C3b receptor (C3bR)-dependent effector functions of macrophages. Enhanced functions of the C3bR were not associated with an increased capability of PMs for intracellular killing of Candida albicans.

Angiotensin II↗

PubMed1983

Effect of angiotensin II on macrophage functions.

Angiotensin II (At II) has been shown to inhibit in vitro the IgG2a-mediated rosette formation of 51Cr-sheep red blood cells (SRBC) by provoked peritoneal macrophages (PM) at 10(-5)-10(-6) M concentrations. The decreased rosette formation was associated with an increased phagocytosis. It was found that the enhanced rosette formation at 10(-7) M hormone concentration was followed by diminished phagocytosis via Fc gamma receptors (R). Processes mediated through Fc microR were affected only after incubation with 10(-5) M of At II. The attachment and subsequent phagocytosis through C3bR was markedly enhanced by At II in a dose-dependent way. Thus, the relative phagocytosis (RP) through both FcRs was significantly enhanced by 10(-5), i.e. by 10(-5)-10(-6) M of At II, but lowered at 10(-7) M hormone concentration. In addition, there was no RP enhancing effect of At II after preincubation with 10(-5) M of indomethacin (IM), indicating the significance of prostaglandins (PG) in the hormone effect. The medium containing 5 mM of EGTA diminished both the RP enhancing and inhibiting effects of At II. The RP mediated by C3b was not affected by At II, IM or EGTA. The intracellular killing capability, measured by chromium release from Candida albicans, was not altered or even slightly diminished after At II treatment of PMs.

Angiotensin II↗

PubMed1981

Effect of lymphokine on the activation and Fc receptor expression of rat macrophages.

Lymphocyte supernatant (LS) containing lymphokine (LK) activated rat peritoneal macrophages (PM) and at the same time enhanced their Fc receptor (FcR) activity. The signs of the early activation could not be observed on alveolar macrophages (AM) but the augmented FcR expression occurred under the effect of lymphokine. The LK-induced macrophage activation and the enhancement of erythrocyte-antibody (EA) rosette formation were found to be independent of each other. In the presence of soybean trypsin inhibitor (STI) the crude lymphokine-induced augmented EA rosette formation was only slightly diminished. However, it did not seem likely that the LK components of molecular weight over 15,000 could enhance the number of rosettes under the effect of protease inhibitor. These data indicate that the macrophage proteases play an important role in the generation of EA rosette formation enhancing breakdown product(s) during the macrophage-lymphokine interaction.

Animals↗

PubMed1981

Role of the cytoskeleton in the Fc receptor activity of rat peritoneal macrophages.

High concentration of cytochalasin B (CB) and vinblastine (Vb) inhibited the erythrocyte-antibody (EA) rosette formation of rat peritoneal macrophages (PM). Low concentration of Vb enhanced rosette formation. CB and Vb had the same effect on the rosette formation when anti-SRBC immunoglobulin (Ig) had been previously bound in vivo or in vitro to the Fc receptors (FcR) of the macrophages, suggesting that the intact function of the cytoskeleton is required for the last step of rosette formation. CB and Vb exert a reversible effect on FcR activity. Regeneration of FcR activity was observed also in the presence of 10 microgram/ml cycloheximide. The effect of CB and Vb on rosette formation depends both on the (sub)classes of antibody involved and on the nature of the particulate antigen. Rosettes with living trypanosomes displayed an extremely high CB sensitivity.

Animals↗

PubMed1981

Effect of angiotensin II on the Fc receptor activity of rat macrophages.

Angiotensin II (At II) in the concentration range of 10(-5) to 5 x 10(-7) M inhibited active and passive erythrocyte-antibody (EA) rosette formation on monolayers of rat peritoneal macrophages (PM) but stimulated it in the range of 10(-7) -10(08) M. Cytochalasin B (CB) and vinblastin (Vb) inhibited the dose-dependent biphasic effect of At II on the Fc receptor (FcR) expression of macrophages. The hormone acts on the last step of rosette formation, i.e. on the binding of sheep red blood cells (SRBC) but does not interfere with the binding of 125I-Ig to FcR. The influence of At II on macrophage rosette formation can be modified by changes in the density of FcR-Ig complexes on the surface of target cells, by the nature of the immunoglobulin (sub)classes involved in rosette formation, and by the biological properties of rosette-forming corpuscular antigen. Based upon the above results we suggest that At II exerts its effect on the contractile elements associated with the cytoskeleton of the macrophage.

Angiotensin II↗

PubMed1980

Fc receptors of rat peritoneal macrophages: immunoglobulin class specificity and sensitivity to drugs affecting the microfilament or microtubule system.

Macrophage-cytophilic antibody activity of various immunoglobulin classes and subclasses was tested in two different rosetting systems. Cytophilic antibody activity of IgM, IgG2a and IgG1 was verified in the SRBC system, while IgM, IgG2a and IgG2c were found to be active in the trypanosome system. Sensitivity to cytochalasin B treatment of SRBC rosette formation was dependent on the class of antibody and decreased in the following order: IgM > IgG1 > IgG2a. Trypanosome rosette formation was prevented by the same drug regardless the type of antibody. Vinblastin caused an enhancement of rosette formation in the SRBC system in low concentration, except when the antibody belonged to subclass IgG1. The enhancing effect was less pronounced in the trypanosome system.

Animals↗

PubMed1976

Endotoxin-induced non-specific resistance in rats examined by Trypanosoma equiperdum challenge.

In rats weighing 100 g, intravenously administered Trypanosoma equiperdum organisms started logarithmic growth immediately, whereas in rats weighing 150-300 g growth started after a lag phase of 0.7-3.1 hr. The lag phase lasted for 15-17 hr when the rats were pretreated serially with endotoxins and this time course was not modified by changes either in the host's body weight or in the germ count of the inocula. Maximum resistance to infection was achieved with gradual doses of the endotoxin given at 48 hr intervals on 6 occasions. The total dose of endotoxin was fourfold of its LD50. Additional doses failed further to increase the resistance. Serial passages of the strain in rats pretreated with endotoxin disclosed that the trypanosomes growing after the lag phase had developed resistance to the factor responsible for the lag phase. Thus the method does not allow a quantitative estimation of resistance induced by serial endotoxin treatment, yet it represents a rapid and simple procedure in every case in which qualitative assessment is sufficient.

Animals↗

PubMed1975