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Biomedical subjects

A Capron

Publications and source records attributed to A Capron.

At least 325 records · Page 18Linked to original sources
PubMed1989

Hypogonadism and ecdysteroid production in Loa loa and Mansonella perstans filariasis.

Possible endocrinological repercussions of infection with Loa loa and Mansonella perstans filariae were studied in Gabonese subjects. Microfilaremic males were compared with amicrofilaremic controls. In the infected group 13/105 subjects (12%) presented only abnormally low serum levels of testosterone (less than 4 ng/ml), 25/105 (24%) only abnormally high serum levels of gonadotrophins, FSH (greater than 15 mIU/ml) and LH (greater than 20 mIU/ml), and 22/105 (21%) presented anomalies in both testosterone and gonadotrophin levels. One out of 68 control subjects had 3.6 ng/ml seric testosterone and all had normal levels of gonadotrophins. Ecdysteroids were detected (greater than 0.025 ng/ml) in the serum of 87/97 (90%) microfilaremic subjects (GM 0.123 ng/ml) compared to 12/64 (19%) controls (GM 0.030 ng/ml). Ecdysteroids were detected in the urine of all subjects, infected (GM 8.468 ng/ml) as well as control (GM 1.245 ng/ml). The hormonal perturbations were correlated with the levels of Loa loa microfilaremia but not with those of serum and urinary ecdysteroids. These results demonstrate that microfilaremic subjects often show endocrinal signs of hypogonadism and present appreciable levels of ecdysteroids in serum and urine. A direct role for parasitic ecdysteroids in hypogonadism remains to be demonstrated.

Adult↗
PubMed1989

Angiostrongylus cantonensis: role of eosinophils in the neurotoxic syndrome (Gordon-like phenomenon).

The role of eosinophils in the pathophysiology of Angiostrongylus cantonensis infections was investigated in nonpermissive (guinea pig) and permissive (rat) hosts. Neurological symptoms similar to the Gordon phenomenon (ataxia, tremor, paralysis) together with a loss of Purkinje cells in the cerebellum were observed after intracraneal injection of human eosinophil extracts or after infection with A. cantonensis, only in guinea pigs and not in rats. Blood eosinophilia as well as eosinophil numbers present in the cerebellum and in the cerebrospinal fluid were higher in guinea pigs than in rats, at all times after infection with A. cantonensis. Increased levels of cytotoxicity toward L3 larvae in vitro were obtained in the presence of guinea pig eosinophils and IgE antibodies, rather than with the corresponding rat effector system. The detection of one eosinophil granule component, the eosinophil peroxidase, in the cerebrospinal fluid from infected guinea pigs but not from rats suggested that in nonpermissive hosts, neurological disorders, similar to the previously described Gordon phenomenon, might be due to eosinophil neurotoxins released after interaction of eosinophils with the parasites.

Angiostrongylus↗
PubMed1989

Development of metacyclic Leishmania promastigotes is associated with the increasing expression of GP65, the major surface antigen.

Using immunofluorescence techniques and flow microfluorometry analysis, we have demonstrated that the binding of a monoclonal antibody (VD5/25) produced against GP65, the major surface antigen of Leishmania braziliensis, increased on the surface of stationary-phase promastigotes from all the New World Leishmania species causing mucocutaneous or cutaneous disease as compared with the log-phase parasites. In addition, a sequential development of Leishmania amazonensis promastigotes from a non-infective to an infective stage was demonstrated. Indeed, promastigotes in the stationary phase (days 6-7) were found to be far more infective than those in the logarithmic phase of growth (day 3) both in vitro for mouse peritoneal macrophages and in vivo for BALB/c mice. The intracellular survival and multiplication of L. amazonensis were significantly inhibited when infective promastigotes were treated with the VD5/25 monoclonal antibody. The increasing expression of GP65 on the promastigote surface may thus contribute to Leishmania infectivity. This seems to represent a characteristic mechanism applicable to all New World Leishmania species studied.

Animals↗
PubMed1989

Molecular basis of host-parasite relationship: towards the definition of protective antigens.

In spite of some remarkable progress in our understanding of the immune response to parasites and in the molecular cloning of dozens of genes encoding for potentially protective proteins, no definitive step has yet been made towards operational vaccines against major human parasitic diseases. The reasons for our present failures are no longer attributable to the lack of appropriate tools but rather to our rather primitive knowledge of the basic mechanisms governing host-parasite relationship. Mainly on the basics of our personal observations, we have attempted to review and discuss some of the prominent factors in host-parasite interactions, such as molecular mimicry, phyletic convergence, molecular mechanisms of infectivity and lures of cell communication. In many respects, the development of efficient vaccines applicable to humans appears closely dependent on a better understanding of the basic biological mechanisms underlying the natural history of parasitic diseases. In this context, the development of new concepts regarding the definition of potentially protective antigens based on the study of non-surface molecules, cross-reactive stage antigens and antibody isotype selection might represent promising alternatives.

Animals↗
PubMed1989

Selectivity of mediators released by eosinophils.

The presence of receptors for IgE on eosinophils has drawn the attention on their direct participation in IgE-dependent hypersensitivity reactions. Surface IgE antibodies were detected on eosinophils from allergic patients. The addition of the specific allergen or anti-IgE antibodies to such purified eosinophils induced the release of eosinophil peroxidase, but not of eosinophil cationic protein. These findings associated with results obtained by using electron microscopy and immunogold staining of the various antibodies directed against the granule proteins allowed us to suggest a selectivity in the mediators released by eosinophils. In addition, preliminary results concerning the existence and the functional role of a receptor for IgA on eosinophils are reported, leading to the concept of a particular interaction of eosinophils with immunoglobulins present in the tissues and their participation in local immune responses.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1989

Inhibition of human eosinophil chemotaxis and of the IgE-dependent stimulation of human blood platelets by cetirizine.

Cetirizine is a new anti-allergic compound with a potent, long-acting, and specific antihistaminic property. Strongly active in the therapy of urticaria and seasonal or perennial rhinitis, it has been shown to inhibit the in vivo eosinophil attraction at skin sites challenged with allergen in atopic patients. In the present work, we confirmed that, at a therapeutical concentration, this molecule had a potent inhibitory action in vitro on eosinophil chemotaxis induced either by N-formyl-Met-Leu-Phe or platelet-activating factor and also on the IgE-dependent stimulation of platelets. These observations appear in favour of a possible role for cetirizine in the modulation of inflammatory cell interactions in allergic processes.

Blood Platelets↗
PubMed1989

IgE and inflammatory cells: the cellular networks in allergy.

The expression by macrophages, eosinophils, and platelets of IgE receptors (Fc epsilon RII) confers on these cells, present or recruited at the site of allergen challenge, a direct role in the development of adverse allergic reactions. The IgE-dependent activation of macrophages, eosinophils, and platelets is moreover inhibited by antiallergic drugs such as disodium cromoglycate or nedocromil. This network of IgE-dependent effector cells is controlled by immunoregulatory pathways which can be target of desensitization therapy. Contrary to their deleterious role in allergic disorders, IgE- and Fc epsilon RII-bearing cells play a decisive role in the immune defense against helminth parasites, therefore pointing to a dualistic function of IgE.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1989

Nedocromil sodium inhibition of IgE-mediated activation of human mononuclear phagocytes and platelets from asthmatics.

The demonstration of a specific receptor for IgE on non-mast cell or basophil leucocytes, such as mononuclear phagocytes, eosinophils and platelets, suggests that these cells may participate directly in immunological disorders of allergy. In this study, inhibition by nedocromil sodium of IgE-dependent activation of human alveolar macrophages, blood monocytes and platelets was investigated. Nedocromil sodium produced an inhibition of IgE-mediated generation of cytotoxic molecules from monocytes and platelets together with a concomitant inhibition of their oxidative metabolism, measured by chemiluminescence. In addition, nedocromil sodium reduced the ability of alveolar macrophages to synthesise and release mediators, estimated by beta-glucuronidase activity. Furthermore, nedocromil sodium inhibited the abnormal response to aspirin of platelets from aspirin-sensitive asthmatics at therapeutic concentrations. These studies confirm that nedocromil sodium acts on a cell compartment other than the classical mast cell population in IgE-dependent allergy and asthma.

Animals↗
PubMed1989

Concomitant augmentation of CD4+ CD45R+ suppressor/inducer subset and diminution of CD4+ CDw29+ helper/inducer subset during rush hyposensitization in hymenoptera venom allergy.

A longitudinal study of patients undergoing rush hyposensitization by honey-bee or yellow jacket venom revealed significant changes of the immunophenotypes until the optimal dose was reached, and a progressive reversion to pre-treatment values in the following months. The activation markers CD23 on B cells and CD25 (IL-2 receptor) on T and B lymphocytes decreased. Although there was little variation of the major CD4 and CD8 lymphocyte populations, CD45R+ cells increased whilst CDw29+ lymphocytes diminished. This inverse variation was associated with a peak of CD4+ CD45R+ cells with concomitant decrease in CD4+ CDw29+ cells showing an inverse effect of the treatment on the reciprocal subsets of CD4 lymphocytes. This indicates a shift in the suppressor/inducer to helper/inducer cell ratio early during rush hyposensitization which may also suggest reversion into a less mature stage of CD4+ cells, associated with the transition from a highly allergen-reactive state to progressive unresponsiveness.

Adolescent↗
PubMed1989

Characterization of a suppressive factor of platelet cytotoxic functions in human and rat schistosomiasis mansoni.

In a previous study we demonstrated that mitogen-stimulated CD8+ CD4-T cells from normal donors produce a suppressive lymphokine (PASL) of IgE-dependent platelet cytotoxicity. Here we demonstrate the production, after antigenic-stimulation, of this suppressive factor during ongoing infections by Schistosoma mansoni in man and in the rat. The T lymphocyte subpopulation producing this factor was also identified as expressing the marker of the suppressive subset. Because of the absence of species restriction, the relevance in vivo of PASL was determined in the rat model. In these conditions we observed a complete abolition of the protection normally conferred against a challenge infection by the passive transfer of platelets from immune to normal rats after treatment of transferred platelets with T lymphocyte supernatants.

Animals↗
PubMed1989

[Infection of T lymphocytes by Trypanosoma cruzi. Possible role of CD3 and HLA-DR].

The mechanisms by which the causative agent of Chagas' disease impair its host's immune response are of paramount importance but poorly understood. Results presented in this paper show for the first time that Trypanosoma cruzi trypomastigotes infect T lymphocytes in vitro and more interestingly in vivo, and that trypomastigotes released from infected cells are infectious. In addition treatment of purified human T lymphocytes with McAb against CD3 and HLA-DR antigens significantly inhibited parasite infection. T. cruzi antigens were detected on the membrane of infected T cells and could therefore represents targets for cytotoxic mechanisms. These results might have important consequences for the understanding of the dramatic disruption of immune response observed during Chagas' disease and more generally provide additional information on T lymphocyte infection by pathogens.

Animals↗
PubMed1989

Immunodeficiencies in parasitic diseases.

Immunodeficiencies linked to parasitism are mainly seen in protozoan infections. The clinical expression varies from generalized unresponsiveness to failure to mount a protective immune response, non-sterilizing immunity being the common situation in most parasite infections. Besides becoming involved with general mechanisms, such as antigenic competition and induction of suppressor cells, parasites can interfere directly in the immune networks through the release of immunomodulatory factors. Antigenic mimicry, antigenic variation at the molecular level (i.e. change in antigen sequence) or topographical level (i.e., surface versus internal expression), and deviation of the immune response towards production of non-protective and even blocking effectors provide unique models of how an infective microorganism can survive and even take advantage of the immune response of its host to reach an equilibrium between host defence and parasite escape strategies responsible for the chronicity of the infection.

Animals↗
PubMed1989

Production of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) in patients with AIDS. Enhanced level of TNF-alpha is related to a higher cytotoxic activity.

We measured simultaneously circulating and cell-generated TNF-alpha and IL-1 after lipopolysaccharide (LPS) stimulation of peripheral blood mononuclear cells (PBMC) by radioimmunoassay (RIA) in HIV-infected individuals at different stages of infection, classified according to CDC classification. TNF-alpha production, both in vitro and endogenous in sera, remained at the normal level in group II patients but was significantly increased in most patients in group IV (P less than 0.05). Most patients of group II and IV displayed normal level of IL-1 in their sera, whereas the level of this monokine generated in vitro was significantly reduced in both groups (P less than 0.05). The cytotoxic effect of factor(s) secreted by PBMC from HIV-infected individuals was evaluated towards a fibroblast cell line L929. The higher titre of cytotoxicity was directly related to a higher production of TNF-alpha by the cells from group IV patients and the effect could be removed by pre-absorption with anti-TNF-alpha monoclonal antibody.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Heterogeneity of human eosinophil glucocorticoid receptor expression in hypereosinophilic patients: absence of detectable receptor correlates with resistance to corticotherapy.

Assessment of steroid receptor content in human neoplastic lymphoid cells or mammary tumour cells has been previously used to predict steroid sensitivity in various types of cancers. In the present study, we have evaluated the relationship between glucocorticoid receptor content and the glucocorticoid sensitivity of human eosinophils, since hypereosinophilic patients do not always respond favourably to glucocorticoid, particularly in the hypereosinophilic syndrome (HES). Blood or alveolar eosinophils obtained from seven patients (four with HES without leukaemic markers; two with parasitic diseases; and one with eosinophilic pneumonia) displayed the same specific glucocorticoid receptor content as normal eosinophils (7.58 +/- 1.31 x 10(3) versus 7.76 +/- 0.74 x 10(3) sites/cell). In contrast, glucocorticoid-binding sites were undetectable in purified eosinophils collected from seven HES patients with (n = 3) or without (n = 4) leukaemic markers, whilst their mononuclear cells and/or neutrophils bound glucocorticoid. In one HES patient, kinetic studies showed that blood eosinophils initially positive in glucocorticoid binding assays became negative with the subsequent appearance of leukaemic markers. The absence of specific glucocorticoid binding sites was correlated with the absence of glucocorticoid receptor proteins by the use of a specific anti-glucocorticoid receptor monoclonal antibody. Eosinophil sensitivity to glucocorticoid was investigated by the evaluation of glucocorticoid inhibition of eosinophil chemotaxis and by the clinical outcome of in vivo glucocorticoid therapy. Our data provide evidence of the heterogeneity of eosinophil glucocorticoid receptor expression. In addition, the presence of glucocorticoid receptors is a prerequisite for glucocorticoid activity, in vitro and in vivo, on cells of the eosinophil lineage.

Drug Resistance↗
PubMed1989

T lymphocyte activation in systemic lupus erythematosus analysed by proliferative response to nucleoplasmic proteins on nitrocellulose immunoblots.

Polyclonal B cell activity in systemic lupus erythematosus (SLE) may be under T cell control. The use of nitrocellulose immunoblots for the analysis of recognition by peripheral blood lymphocytes of nucleoplasmic proteins in SLE patients led to the characterization of significant proliferative responses to 68K (U1 RNP); SS-B; B-B' and D (Sm) antigen in 15 of 20 patients. Variations of proliferative response were parallel to disease activity over a follow-up period of greater than or equal to 6 months, conferring some prognostic value to the assay of lymphocyte response to nucleoplasmic antigens. The pattern of reactivity differs from the corresponding serum antibody profile, and purified T cell suspensions (greater than 95% pure) were shown to proliferate in response to soluble nucleoplasmic antigens, indicating that T and B cell repertoires against nucleoplasmic proteins may differ. This suggests that activated helper T cells contribute to the fine modulation of B cell reactivity to subcellular particles to determine the particular antibody profile of the patients.

Adolescent↗