[Disorders of hepatic glycogen phosphorolysis during histamine poisoning].
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Glycogen↗
Biomedical subjects
G Cordier
Publications and source records attributed to G Cordier.
Visna-maedi virus-induced expression of interleukin-8 gene in sheep alveolar cells following experimental in vitro and in vivo infection.
Visna-maedi virus is a lentivirus which causes inflammatory disorders in sheep, including a chronic interstitial lung disease resembling that observed in human immunodeficiency virus type 1 (HIV 1) infection. In view of our previous demonstration of the production of neutrophil chemotactic activity by alveolar macrophages, and given the lymphocytic and neutrophilic nature of the alveolar cell infiltrate in both naturally and experimentally infected animals, we hypothesized that interleukin-8 (IL8) could be a candidate for at least part of the chemotactic activity we described. In this study, we investigated IL8 mRNA expression following visna-maedi virus infection. Northern analysis of total RNA using an ovine IL8-specific probe demonstrated that the IL8 gene is upregulated in alveolar macrophages as a consequence of in vitro infection and in alveolar cells from experimentally infected animals. Using a semi-quantitative RT-PCR method, we showed that various levels of IL8 mRNA are expressed by alveolar cells from infected animals and that they correlate with the intensity of the lesions. In conclusion, visna-maedi virus is able to induce IL8 mRNA expression in sheep alveolar cells. Results from in vivo infected animals suggest that IL8 could play a role in the early build-up of visna-maedi virus-induced lesions.
Animals↗
Heterogeneity of human B lymphocytes as revealed by monoclonal antibodies.
Two monoclonal antibodies directed at determinants on human B lymphocytes were produced and characterized by indirect immunofluorescence. The antibodies, BL13 and BL14, were found to be specific for B cells, since they did not react on red cells, platelets, granulocytes, monocytes or T lymphocytes. BL14-associated antigen was present on most of the circulating and tissular B cells, whereas that detected by BL13 was mainly restricted to a subpopulation preferentially homed in germinal centers of secondary follicles of lymph nodes and tonsils, which did not circulate under normal conditions and disappeared once B cells were activated by mitogens. Immunoprecipitation studies demonstrated that BL13 precipitated an antigen of approximately 160,000 d. Pathological studies confirmed the specificity of BL13 and BL14 antibodies for B lymphocytes, since they never reacted with non-B malignancies. BL14 bound to nearly all malignant B-cell proliferations except very immature and plasmacytoma cells. In contrast, BL13 was always found to be negative on acute lymphocytic leukaemias, prolymphocytic leukaemias, hairy cell leukaemias and plasma cells, whereas it detected 40-50% of chronic lymphocytic leukaemias and Burkitt or non-Burkitt lymphomas. These results led us to hypothesize several compartments for B-lymphocyte differentiation, either in central (bone marrow) or peripheral lymphoid organs, with BL13 antibody defining one compartment in the germinal centers.
Antibodies, Monoclonal↗
Increased expression of tissue factor mRNA and procoagulant activity in ovine lentivirus-infected alveolar macrophages.
To link ovine lentivirus infection to lung tissue damage, we studied the procoagulant response in alveolar macrophages from experimentally infected lambs and in in vitro infected alveolar macrophages. We cloned ovine tissue factor cDNA and analysed its in vitro expression by Northern blotting. Visna-maedi virus induced tissue factor mRNA. In order to correlate this mRNA induction with its cellular function, we analysed macrophage procoagulant activity after in vitro and in vivo infection. The procoagulant activity was increased by interaction with the virus in both cases. Thus, visna-maedi virus-induced expression of tissue factor mRNA was associated with enhanced macrophage procoagulant activity. These findings indicate an active role of alveolar macrophages in the pathogenesis of these inflammatory lung lesions.
Animals↗
[Tricho-rhino-phalangeal syndrome: 2 sibling groups].
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Abnormalities, Multiple↗
[Plunging goiters, thoracic goiters. Apropos of 67 cases].
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Female↗
Bronchoalveolar lavage in radiation pneumonitis.
Bronchoalveolar lavage (BAL) was carried out in six patients with radiation pneumonitis, the early radiation-induced lung damage that usually leads to radiation fibrosis. Protein analysis by immuno-electrophoresis and polyacrylamide gel electrophoresis of BAL fluid revealed leakage of circulatory proteins, including high molecular weight components. Cell count of BAL fluid showed an increased number of lymphocytes; these proved to be activated on cell cycle analysis in one patient. Collagenolytic activity, assessed by degradation of radiolabelled type I human collagen, was present in BAL fluid of all six patients. The following mechanisms are therefore considered to participate in the pathogenesis of radiation-induced lung damage: 1) permeability oedema, which led to acute respiratory distress syndrome in one case of hyperacute radiation pneumonitis, 2) lymphocyte alveolitis possibly perpetuated by activated lymphocytes, and 3) release of collagenolytic enzymes in alveolar structures contributing to fibrotic processes.
Bronchi↗
[Alpha 1-antitrypsin/lymphocyte interactions: cytofluorometry study].
Purified alpha 1-antitrypsin (alpha 1AT) was previously shown to prevent primary antibody response and lymphocyte DNA synthesis. We have reported that radiolabelled alpha 1-AT could bind to human lymphocytes and inhibit surface proteolytic activity. However, the radiolabelling method brings no information on the eventual heterogeneity of alpha 1AT distribution among the population nor on the presence of alpha 1AT on untreated lymphocytes. In this report, we have investigated these two points using indirect fluorescence followed by flow cytofluorometric analysis. The presence of alpha 1AT was revealed on a variable percentage of untreated peripheral blood and tonsillar lymphocytes. The incubation of cells with additional alpha 1AT induced an increase of the percentages of fluorescent lymphocytes. This binding was specific and could be inhibited by pretreatment with the protease inhibitor tosyl-L-phenylalanine-chloromethyl-ketone (TPCK) (2 X 10(-5)M). Furthermore, TPCK and EDTA (3 mM) could displace alpha 1AT initially bound to the lymphocyte surface.
Cell Separation↗
Distinct functions of surface receptors in the induction of neutrophil-mediated cytotoxicity.
The respective roles of cell surface receptors were studied in a model of cell-mediated cytotoxicity using 51Cr-labelled chicken erythrocytes as target cells and human polymorphonuclear neutrophils (PMN) as effector cells. The attachment of the targets to PMN, demonstrated by rosette formation, was achieved by PMN surface receptors for C3 or for Fc IgG. No receptors for Fc IgM could be demonstrated. Direct contact between targets and effector cells was required and no cell-free cytotoxic mediator was demonstrable in this model. Target cells bound to PMN-C3 receptors were not lysed unless a cytotoxicity inducing signal was delivered. This was provided by anti-PMN heteroantibodies, or by their F(ab')2 fragments as well. It was therefore possible to trigger the cytotoxic reaction by bypassing PMN-surface receptors for Fc IgG. When the target cells are coated with IgG antibodies, PMN receptors for Fc IgG ensure both the attachment and the triggering signal for the cytotoxic reaction. Polymorphonuclear neutrophils (PMN) have been reported to the effective killer cells in vitro under three different experimental conditions: during phagocytosis, in the presence of antibody directed against the target cells and in the presence of lectins. PMN accumulation has also been considered as a major component of the pathogenesis of many forms of immunologic tissue injuries since PMN may react with immune complexes bound to a surface which they cannot phagocytose. Under these circumstances, they release lysosomial enzymes, by a mechanism which has been called "reverse endocytosis" or "frustrated phagocytosis". Attachment of PMN to target involves cell surface receptors (Fc gamma R) for the Fc region of the IgG molecule and/or receptors (C3R) for the activated third component of complement. The binding of aggregated or antigen-complexed IgG to PMN surface Fc gamma R generates signals triggering the internalization phase of phagocytosis, the antibody-dependent cell cytotoxicity (ADCC) and the stimulation of glucose oxidation by the hexose monophosphate pathway. However, the latter metabolic activation was also reported to be triggered by the fixation of antibodies specific for PMN surface determinants. It was therefore conceivable that modifications induced at the membrane level on any structure distinct from Fc gamma R would produce metabolic changes leading to target cell destruction, provided that a close contact could be established between effector and target cells. In the present study we have investigated the respective roles of Fc gamma R, C3R and other yet undefined surface determinants of PMN in the induction of cytotoxic activity towards heterologous target cells.
Animals↗