Biomedical subjects

A Capron

Publications and source records attributed to A Capron.

At least 487 records · Page 27Linked to original sources

PubMed1985

[Evaluation of radioimmunoassay for antithyroglobulin autoantibodies].

A statistical analysis is performed on the results of 881 determinations of thyroglobulin antibodies in humans. Antibodies were assayed comparatively by radioimmunoassay using a sandwich method and by tanned red cell haemagglutination. A very good concordance was found between the two techniques, apart from the low titer zone. A significant correlation was observed between on the one side, the radioactivity index of the diluted serum, defined as the increment of radioactivity bound by undiluted patient serum over the positive threshold, divided by this threshold, and, on the other side, the antibody titer, i.e. the reciprocal of the highest serum dilution superior to the positive threshold by radioimmunoassay. The corresponding linear regression allows to define a arbitrary unit system which associates values of the radioactivity index with an average antibody titer.

Autoantibodies↗

PubMed1985

[IgE antibodies in human Fasciola hepatica distomiasis].

In patients infected by Fasciola hepatica, total IgE and specific IgE antibodies have been determined by radioimmunoassays, and IgG, IgA, IgM levels by radial immunodiffusion test (Mancini, 1965). Moreover, total and specific IgE levels have been related to parasite egg burden, age, clinical features and eosinophilia. Elevated total IgE and specific IgE antibodies levels have been found respectively in 76% and 48% of the patients whereas there was no significant variations in other immunoglobulins levels. However, though the amount of total and specific IgE was lower than in other helminthic diseases, it appears to be a significant data of the immune response to parasites as it has been reported and discussed previously. It has been shown a significant relationship between total and specific IgE levels, the number of lines by immunoelectrophoresis, and the results of the indirect haemagglutination and indirect fluorescent antibody techniques; each method appeared to be in equal value to perform the early diagnosis of human Fasciola hepatica. In addition, specific IgE antibodies levels were correlated with eosinophilia specially when it exceeds 15%. This results demonstrate the availability of their measurement in the diagnosis of fascioliasis versus other diseases with marked eosinophilia.

Eosinophilia↗

PubMed1985

[Demonstration of specific platelet function anomaly in asthma induced by aspirin: diagnostic consequences].

Aspirin-sensitive asthma is a common and severe disorder characterized by asthmatic attacks after oral ingestion of cyclooxygenase inhibiting drugs. Yet its pathophysiology remains unknown, and no specific in vitro abnormality, neither humoral nor cellular, has been detected in these patients. We have recently described a new model of platelet activation--IgE-dependent platelet activation--expressed by the release of cytocidal mediators and oxygen metabolites. We have now investigated whether cyclooxygenase inhibitors induce a similar response in platelets from aspirin-sensitive asthmatics in vitro. Aspirin or indomethacin strikingly activated platelets from 12 aspirin-sensitive asthmatics to the same extent as IgE-dependent stimuli, but had no effect on platelets from 18 controls (p less than 0.0001). Sodium salicylate, which does not inhibit cyclooxygenase, did not trigger platelets from aspirin-sensitive asthmatics. Preincubation with sodium salicylate or prostaglandin endoperoxides (PGH2), selectively prevented further platelet activation by aspirin or indomethacin (90% inhibition), suggesting that this abnormal platelet activation is the consequence of cyclooxygenase inhibition. This represents the first identification of a specific abnormal cellular response in aspirin-sensitive asthma, provides the basis for an in vitro diagnostic test of the disease, and for new insights on its pathogenesis and its prevention.

Aspirin↗

PubMed1985

Extracellular release of rat eosinophil peroxidase (EPO) I. Role of anaphylactic immunoglobulins.

The release of intracellular peroxidase (EPO) was investigated in order to evaluate rat eosinophil activation by various immunoglobulin (Ig) isotypes. After successive incubations with purified rat IgG1, IgG2a, IgG2b, IgG2c, IgE, or IgM and their respective anti-Ig antisera, eosinophils released significant amounts of EPO (up to 26% of the intracellular content) only in the case of Ig with anaphylactic activities (IgG2a and IgE). Other classes and subclasses were unable to induce EPO exocytosis. Selective depletion and reconstitution experiments suggested that mast cells were not required in this process. Similar levels of EPO could be released after interaction of eosinophils with antigen-antibody complexes (IgG2a monoclonal antibody and Schistosoma mansoni antigen) immobilized on nonphagocytosable surfaces. These results indicate that EPO exocytosis can be obtained after cell activation with specific antibodies, and that this mechanism is independent of phagocytosis. A kinetic study of eosinophils from S. mansoni-infected rats revealed that IgG2a and IgE cytophilic antibodies induced EPO release after incubation with either specific antisera or specific antigen, which suggests the in vivo relevance of such findings. The present work underlines the parallelism of interaction of anaphylactic-type Ig with eosinophils and with mast cells. Moreover, EPO release seems to represent an interesting marker of eosinophil activation, because close relationships were established between the present findings and previous work on the effector function of rat eosinophils.

Anaphylaxis↗

PubMed1985

The use of monoclonal antibodies in studies of filarial parasite antigens.

The strength of the hybridoma technology in providing probes for the study of parasite immunology is obvious. The use of monoclonal antibodies should greatly expedite the task of the identification and the isolation of antigens which are relevant to host protection, of immunodiagnosis and of immunopathology. We have produced a series of monoclonal antibodies against Brugia malayi which causes lymphatic filariasis in man. One of these monoclonal antibodies (IgM isotype) can detect circulating antigens in the sera of individuals and of laboratory animals infected with B. malayi by radioimmunoprecipitation-PEG assay. This monoclonal antibody can bind to the relevant epitope of the circulating antigen or to the antigenic determinants of the immune complexes that remained exposed in the complex. A few monoclonal antibodies raised against B. malayi were selected, one of which gave positive fluorescence reaction on the surface of microfilariae. This particular monoclonal antibody showed such biological activities as conferring resistance to circulating microfilariae and inducing cell-mediated killing of microfilariae in vitro. The same monoclonal antibody was able to identify antigenic determinants (of mol. wt, 110 Kd) on the surface of B. malayi microfilariae which may be involved in effector mechanisms related to the development of transmission inhibiting immunity in lymphatic filariasis.

Animals↗

PubMed1984

Excretion of ecdysteroids by schistosomes as a marker of parasite infection.

Ecdysteroids produced by schistosomes are released in biological fluids of infected hosts. In the sera, the concentration of ecdysteroids correlates with the permissiveness of the host to schistosome infection and its detection is available in the absence of positive parasitological tests. In the urine, ecdysteroid concentration decreases markedly after chemotherapy. 20-Hydroxyecdysone and its epimer were identified in the urine of infected patients using mass spectrometry. These data demonstrate for the first time that ecdysteroids are released by organisms. Moreover, they are potent molecules of parasite infection and can be used for parasite diagnosis.

Adolescent↗

PubMed1984

Rat IgE directed against schistosomula-released products is cytotoxic for Schistosoma mansoni schistosomula in vitro.

The immunogenicity of molecules shed by schistosomula into culture medium (antigens present in schistosomula-released products, SRP-A) has been studied. The results obtained show that SRP-A preferentially induce an IgE response when injected into rats, without the need for adjuvants. Moreover, anti-SRP-A IgE is cytotoxic in vitro for the larvae in the presence of macrophages, eosinophils or platelets, which have previously been demonstrated as being the three efficient killer cells for schistosomula in the presence of specific IgE. Immunofluorescence analysis locates the target antigens at the schistosomulum surface. Among the antigens recognized by anti-SRP-A IgE, two molecules of 26 and 22 kDa have been identified by sodium dodecyl sulfate polyacrylamide gel electrophoresis followed by western blotting.

Animals↗

PubMed1984

Interactions between eosinophils and antibodies: in vivo protective role against rat schistosomiasis.

An original protocol of cell transfer from Schistosoma mansoni-infected rats to normal recipient rats is used to investigate the protective role of phagocytic cell populations, described as effector cells in vitro, against a challenge infection with S. mansoni. Nonadherent, eosinophil-enriched and -adherent, macrophage-rich cell preparations, injected via intradermal and subcutaneous routes at the precise site of exposure to cercariae, were able to significantly protect the recipient rats. The time-course study of this protective effect according to the time after infection of donor rats revealed that eosinophils were the major cell population involved in the early phase of infection (4 to 5 weeks), whereas macrophages could also be incriminated thereafter. A rosette assay using anti-immunoglobulin-coated erythrocytes indicated a sequence of the various antibody isotypes under study (IgG1, IgG2a, IgE) on the eosinophil surface, during the course of infection. As previously shown in vitro, cytophilic antibodies seemed to participate in the protective effect of eosinophils, since eosinophil-enriched cells from normal rats, sensitized in vitro with immune complexes present in infected rat serum, could also confer significant protection. These observations establish therefore the relevance between our previous in vitro studies and rat resistance to a challenge infection with S. mansoni, underlining the major role played by the interaction between antibodies and phagocytic cells (eosinophils and macrophages).

Animals↗

PubMed1984

Influence of vitamin A on the immune response of Schistosoma mansoni-infected rats.

Nutritional (vitamin A levels, weights), parasitological (adult worm burden, count of eggs in liver, stool examination) and immunological (IgE serum levels, anti-Schistosoma mansoni antibodies, lymphocyte stimulation by concanavalin A and S. mansoni antigenic extract) parameters were studied in three groups of rats, a non-infected and normally fed control group, a S. mansoni-infected but normally fed group, and a S. mansoni-infected group with experimentally induced vitamin A deficiency. The number of worms was found significantly higher in the third (53 +/- 19) than in the second group (2 +/- 2) (p less than 0.001). There were many eggs in the liver surrounded by granulomatous reactions in the third group (399 +/- 73 epg liver). All stool examinations were negative. IgE levels and anti-S. mansoni antibody titres were significantly lower (p less than 0.001) in the third than in the second group. The concanavalin A lymphocyte stimulation indexes did not differ significantly between groups 2 and 3; the S. mansoni lymphocyte stimulation index was only significantly positive in group 3 (p less than 0.001). These results indicate a decrease in the humoral immune response without alteration of cellular immune response in vitamin A-deficient rats infected with S. mansoni.

Animals↗

PubMed1984

Filaricidal effects of cyclosporin-A against Dipetalonema viteae in Mastomys natalensis.

Outbred male Mastomys natalensis were injected subcutaneously with 100 infective larvae of Dipetalonema viteae obtained from Ornithodorus tartakovskyi. Groups of five animals were treated with 30 mg/kg of the immunosuppressive drug Cyclosporin-A daily for five days (experimental) or Miglyol 812 (control). One group served as untreated controls. Contrary to expectations, 60% of the animals were completely protected against D. viteae and the remainder were partially protected. The mechanism remains unknown.

Animals↗

PubMed1984

Secretion of a chemotactic factor for neutrophils and eosinophils by alveolar macrophages from asthmatic patients.

The studies presented in this article demonstrate the release of an IgE-dependent chemotactic factor for polymorphonuclear neutrophils (PMN) and eosinophils by alveolar macrophages (AMs) from normal subjects (n = 15) and allergic asthmatic patients (n = 15). A 60-minute incubation of normal AMs previously sensitized by 20% nonheated allergic sera with anti-human IgE antibody or the related allergen induced the release of a chemotactic activity (CA) for PMN and eosinophils in culture supernatants. When AMs were obtained from asthmatic patients, direct incubation with anti-IgE or the related allergen induced the same CA, whereas incubation with an unrelated allergen failed to produce CA (neutrophil CA after addition of anti-IgE, 22.5 +/- 3.5 cells per high power field; with related allergen, 15.8 +/- 3.6; with unrelated allergen, 0.7 +/- 1.8; p less than 0.0001). A partial characterization of the neutrophil chemotactic factor was carried out. Enzymatic treatment by trypsin or carboxypeptidase or by heating (56 degrees C for 3 hr) failed to abolish the neutrophil CA. After gel filtration the greater part of the neutrophil CA (80%) was recovered among low-molecular-weight components (300 to 1300 daltons). A preliminary deactivation of PMN by leukotriene B4 suppressed the CA of AM supernatants. These results indicate that IgE-dependent stimulation of AMs produces a neutrophil and eosinophil CA, present in a low-molecular-weight fraction possibly related to leukotrienes, and emphasizes the role of AMs in inflammatory lung processes during allergic asthma.

Adult↗

PubMed1984

Occurrence of fibronectin antigenic determinants on Schistosoma mansoni lung schistosomula and adult worms.

Fibronectin determinants were revealed in a soluble extract of Schistosoma mansoni adult worms by standard immunodiffusion and immunoelectrophoresis techniques. The same target molecules were demonstrated on the parasite's surface using a binding assay with [125I] anti-fibronectin. The use of fluorescein- and peroxidase-conjugated-antibodies confirmed the above observations and provided a fairly precise means for locating the cross-reacting antigen on the worm surface. An in vitro cytotoxic assay using inactivated (56 degrees C, 2 h) anti-fibronectin rabbit immune serum and guinea-pig serum as a source of complement was developed. In these conditions, anti-fibronectin exerted cytotoxic activity against lung schistosomula and adult worms but not skin schistosomula. The ultrastructural damage induced by anti-fibronectin in the presence of complement was studied using transmission electron microscopy. The results suggest a close association between fibronectin determinants and S. mansoni membrane.

Animals↗

PubMed1984

Human antibody response to Schistosoma mansoni surface antigens defined by protective monoclonal antibodies.

The antibody response to a 38,000-dalton schistosomular surface antigen, defined by a rat protective monoclonal antibody and specific for Schistosoma species, has been studied in a group of 125 Brazilian patients with schistosomiasis. Antibodies binding this particular antigen were detected in 97% of patient serum samples, a result suggesting that it could represent a potent immunogen. Quantitative studies of the amount of isolated antigens were performed in relation to the age of patients. Results showed a maximal response in the second decade of life and correlated with previous observations on the prevalence and intensity of schistosomiasis. However, in the present study no relationship was shown between the binding capacity of sera and the number of schistosomal eggs in individual patients. These data suggest that the antibody response to the 38,000-dalton schistosomular antigen could be a marker of infection by schistosomes.

Adolescent↗

PubMed1984

Non-specific potentiation of T- and B-lymphocyte proliferation at the early stage of infection by Schistosoma mansoni: role of factors secreted by the larvae.

The response of rat lymphocytes to schistosomula released products (SRP) was examined. SRP non-specifically activated lymphocytes by potentiating their proliferative response to PHA, Con A or LPS. The parasite factor involved was dialysable and heat stable. The addition of SRP to cultures containing nylon-wool non-adherent lymph node cells resulted in a significant enhancement of cell proliferation. The effect of SRP on athymic nude (Nu/Nu) and litter mate (Nu/+) control rat cells indicated an effect on the proliferation of both B and T lymphocytes. SRP acted in a dose-dependent manner and its action was observed as early as the beginning of cell division. This corresponds to the in vivo situation, since at the early stage of infection increased proliferative responses of the lymph node cells to mitogens were observed. The adjuvant effect of SRP could partly explain the regulation of the cellular immune response observed during S. mansoni infection by the parasite itself and could represent one of the mechanisms involved in immunity to reinfection that is under the control of the parasite.

Animals↗

PubMed1984

Humoral and cellular immunity in patients with hepatic alveolar echinococcosis. A 2 year follow-up with and without flubendazole treatment.

Parameters of humoral and cellular immunity were assessed in 12 patients with alveolar echinococcosis (AE) of the liver before, during and after discontinuation of treatment with flubendazole (FZ). In infected patients, before any medical treatment values of serum IgG, IgA, total haemolytic complement and C4 were significantly higher than those observed in control subjects; IgA levels were higher in jaundiced patients. Specific antibodies assayed by indirect haemagglutination and immunoelectrophoresis were present only in infected patients and were shown to decrease by the sixth month of treatment; however, similar fluctuations were observed without treatment. The percentage and absolute number of B lymphocytes, and total circulating lymphocytes, were significantly lower in patients with AE. An impairment of functional activity of T cells assayed by the leucocyte migration test, with PPD and Candidin as antigens, was demonstrated despite a normal percentage of SRBC rosettes. The 'score' of migration index still decreased during FZ treatment and returned to initial values after the year of follow-up without treatment. These results suggest that human AE is associated with important immunological disturbances. Changes in humoral immunity can be unequivocally considered to be a consequence of the parasite infection. The primary or secondary nature of the impairment of cellular immune responses and its mechanisms remain to be elucidated. Flubendazole could be responsible for an increase of cellular immune alterations in these patients.

Adult↗

PubMed1984

Inhibition of primary and secondary IgE-response by a schistosome-derived inhibitory factor.

Schistosome-derived inhibitory factor (SDIF) previously shown to inhibit lymphocyte proliferation, markedly decreased the primary IgE response of rats immunized with dinitrophenylated ovalbumin (DNP-OVA) when injected either simultaneously or shortly after antigen administration. No effect however was observed when SDIF was injected before the immunization. An inhibition of non-IgE anti-DNP antibodies was also found in SDIF-treated rats although the decrease was lower than with IgE antibody. IgE responses of both low and high IgE responder rats were reduced but a lower dose of SDIF was required in the case of high IgE responder Brown Norway rats. When SDIF was only given at the time of priming, the secondary IgE response was no longer modified. However, the administration of SDIF together with the second injection of the antigen induced marked decrease in the secondary IgE response. The effects of SDIF on primary and secondary IgE responses could be attributed to the inhibitory activity of the parasite-derived factor on lymphocyte proliferation. The observed inhibition of secondary IgE antibody responses confers to SDIF a pharmacological interest in allergic diseases.

Animals↗

PubMed1984

Different monoclonal antibodies against the component 5 specific for Trypanosoma cruzi.

Three murine monoclonal antibodies (I-35/67, II-190/30, III-160/18) produced by immunization against total epimastigote extract or component 5-enriched fractions of Trypanosoma cruzi (Tehuantepec strain) have been demonstrated to recognize the component 5 specific for T. cruzi. By immunofluorescence studies, one of these monoclonal antibodies (I-35/67) was shown to bind to the epimastigote cell surface, and the two others (II-190/30 III-160/18) were preferentially directed against internal subcellular organelles. Immunoprecipitation using these monoclonal antibodies followed by SDS-PAGE analysis, has led to identification of four molecules with apparent molecular weights of 72 Kd, 51 Kd, 43 Kd, and 24 Kd in T. cruzi epimastigotes. Potential uses of these monoclonal antibodies in serological tests and immunochemical analysis of target antigens are discussed.

Animals↗

PubMed1984

Macrophage triggering by aggregated immunoglobulins. II. Comparison of IgE and IgG aggregates or immune complexes.

Macrophages incubated with complexed or aggregated IgE released beta-glucuronidase (beta-G) within 30 min. In contrast in the presence of aggregated or complexed IgG, macrophages liberated equivalent amount of beta-G only after 6 h incubation. In addition the rapid macrophage stimulation induced by aggregated IgE was also followed by a faster 3H-glucosamine incorporation when compared to the delayed activation caused by aggregated IgG. However, macrophages stimulated either by IgG or by IgE oligomers produced the same percentage of plasminogen activator at 24 h. In contrast, while the interaction between macrophages and aggregated IgE was only followed by a peak of cyclic GMP and a beta-G release during the first 30 min of incubation, the interaction between macrophages and IgG oligomers was accompanied by a simultaneous increase of cyclic GMP and AMP nucleotides and by an absence of beta-G exocytosis. Moreover, the beta-G release induced by aggregated IgE was increased when macrophages were preincubated with aggregated IgG. This additive effect was not observed in the reverse situation. Finally macrophages activated by IgG oligomers were demonstrated to exert a cytotoxic effect on tumour cells and to kill schistosomula in the presence of a low level of complement. Taken together these results underline the peculiar ability of aggregated or complexed IgE to trigger rapidly the macrophage activation compared to aggregated IgG and can explain the important role of complexed IgE in some macrophage dependent cytotoxicity mechanisms (i.e. in parasitic diseases).

Animals↗