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Biomedical subjects

B Csaba

Publications and source records attributed to B Csaba.

At least 19 recordsLinked to original sources
PubMed1991

Dynamics of 125I-labelled horse serum albumin presentation in vivo in guinea pigs.

Low antibody production in guinea-pig sera was determined by passive hemagglutination after 125I-labelled horse serum albumin (HoSA) injection. The appearance of radiolabelled HoSA on T cells, B cells and monocytes/macrophages (Mo) of guinea pigs was detected and followed as a function of time. The radioactivity peaks appeared first on B cells and Mo, later on the T cells. The circulating T lymphocytes contained labelled antigen 7 days after the injection while T and B lymphocytes in the spleen preserved their radioactivity 15 and 20 days later. Helper, suppressor and effector T cells were able to fix 125I-HoSA, this was shown by autoradiography using monoclonal antibodies 4 days following the antigen injection.

Animals↗
PubMed1988

Antigen-specific lymphocyte clone elimination and reappearance in guinea pigs using 125I-labelled horse serum albumin.

T cells in the blood and spleen of guinea pigs fixed significantly higher quantities of radiolabelled antigen on day 4 following injection than did B cells or macrophages. Fixed radioactivity produced continuous radiation damage on the cells involved and the antigen-specific lymphocyte clone disappeared. This was shown by the absence of antibody production in the sera determined by passive haemagglutination. The reappearance of the specific lymphocyte clone required more than 20 days.

Animals↗
PubMed1985

Inhibition of anaphylaxis by inactivated lymphocyte clone with radiolabelled antigen.

125I-labelled ovalbumin (OVA) antigen did not sensitize guinea-pigs and anaphylaxis did not develop after native OVA challenge. The radiolabelled antigen was fixed by lymphocytes with highly specific receptors for 125I-OVA and this condition produced a continuous radiation damage leading to inactivation of the cells. As the proliferative response of lymphocytes did not occur, no antibody production was detected. This was demonstrated by passive haemagglutination techniques. However, the immune response to a simultaneously given non-radioactive antigen remained intact. It is supposed that radiation damage depended on specific activity of antigen destroying the antigen-specific lymphocyte clone selectively. The mechanism and the practical importance of the in vivo 'antigen suicide' is discussed.

Anaphylaxis↗
PubMed1979

Effects of disodium chromoglycate on systemic anaphylaxis in guinea pigs, rats and mice.

Disodium chromoglycate (DSCG) exerted a protective action in passively-sensitized guinea pigs undergoing anaphylaxis but no such effect was found in actively-sensitized animals. The degree of protection depended on the route and the time of administration. DSCG also protected actively-sensitized rats undergoing anaplylaxis but no effect was found in mice.

Anaphylaxis↗
PubMed1979

Detection of thymosin 5 in calf and mouse thymus and in nude mouse dysgenetic thymus.

Thymosin 5 was traced in calf and mouse thymuses by fluorochrome-labelled rabbit anti-calf thymosin. The presence of thymosin 5 or its individual components was found 1. in groups of cortical epithelial cells in calf thymuses and in single cortical epithelial cells in mouse thymuses. 2. In some marginal (blastema) cells of the thymus cortex of calves and 14-day-old mice. 3. In perivascular epithelial cells of the calf thymus. 4. In occasional medullary epithelial cells of the calf and mouse thymus. In all cases there was a marked alternation of entirely negative and positive cell-containing thymic lobuli. In 4 of 13 cases comparatively strong positivity was found in tightyly arranged epithelial cells in an individual acinus in the dysgenetic thymus of nude mice, the positive cases being concentrated among the youngest mice studied.

Animals↗
PubMed1979

Functional heterogeneity of macrophages.

The antibody-binding activities of rabbit peritoneal macrophages separated on discontinuous gradients of Ficoll were investigated. The antibody was rabbit anti-ovalbumin IgG labelled with 125I. Of the five fractions obtained, one macrophage fraction was found to bind substantially more antibody than the others. These macrophages possessed more Fc receptor sites than the others and the number of Fc receptors (n) and the association constant (K) of these cells was calculated. By electron microscopy, the phagocytic activity of the subpopulation with most Fc receptors was less than that of the others.

Animals↗
PubMed1977

Platelet activating factor, the trigger of haemostatic alterations in rat anaphylaxis.

Platelet-activating factor (PAF) generated by an IgE-mediated reaction in the peritoneal cabity of rats was partially purified by adsorption to diatomaceous earth. It aggregated rat platelets and, as a consequence, activated Hageman factor in in vitro, as well as in vivo, conditions. The haemostatic alterations induced by PAF showed similarity to those observed in the early phase of rat anaphylaxis.

Anaphylaxis↗
PubMed1976

Platelets in rat anaphylaxis.

The number of circulating platelets dropped abruptly in the early phase of severe anaphylactic shock (AS) of the rat and could be inhibited by Persantin but not by heparin pretreatment. The results strongly suggest that an aggregating agent, perhaps "platelet aggregating factor", formed or released during anaphylaxis is responsible for the decrease of platelet number. The organ distribution of 51Cr labelled platelets showed that in AS the aggregated platelets were removed from the circulation mostly by the spleen and part of them were trapped in the lung and the small intestine. The remaining platelets retained their functional integrity. The loss of circulating platelets is manifested by the prolongation of rat tail bleeding time and is one of the factors participating in the haemostatic disturbances during anaphylaxis.

Anaphylaxis↗
PubMed1976

The fixation of heterocytophylic antibodies to macrophages.

Using autoradiographic methods, heterocytophylic antibodies were found to be fixed to the peritoneal macrophages of the guinea pig. The heavy chain of the IgG molecule was responsible for the cell fixation which was inhibited by the autologous Fc fragment. The fixation of heterocytophylic immune complex (rabbit antibody IgG + homologous OA antigen) was also inhibited by the Fc fragment. Only some of the macrophages (35-50%) were able, however, to fix immune complex.

Animals↗
PubMed1976

Activation and consumption of Hageman factor in the anaphylactic shock of the rat.

In the early stages of anaphylactic shock of rats pretreated with Bordetella pertussis vaccine, a prompt and parallel activation of the factor XIIa-dependent intrinsic coagulation, kinin generation, and fibrinolytic acticity was observed. The coagulation studies, the similarity of anaphylactic results with those produced by a single injection of ellagic acid, and the effective inhibition of the anaphylactic and the ellagic acid-induced activation of these pathways by lysozyme all suggest that factor XII itself becomes activated in rat anaphylaxis. As the reaction proceeded, considerable anticoagulant activities emerged, but the bradykinin and the plasminogen activator levels even further increased. During the first 10 min of anaphylactic shock, factor XII was partly consumed and this was prevented by epsilon-aminocaproic acid infusion. The results show that in pathological conditions such as anaphylaxis there is an intimate in vivo interaction among the three factor XIIa-dependent pathways.

Aminocaproates↗
PubMed1975

Evidence of fibrinogen degradation in rat anaphylaxis.

In active anaphylactic shock of rats pretreated with Bordetella pertussis vaccine, both plasma thrombin clotting time and the amount of antigenically active fibrinogen degradation products in the serum were increased. The formation of clottable fibrinogen fragments was shown by SDS polyacrylamide gel electrophoresis of thrombin-induced clots. When plasma of rats pretreated with 125I rat fibrinogen and then subjected to anaphylaxis was submitted to SDS polyacrylamide gel electrophoresis, fibrinogen-split products were also detected. Fibrinogen degradation results from the proteolytic effect of an activated fibrinolytic enzyme.

Anaphylaxis↗