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B Descamps-Latscha

Publications and source records attributed to B Descamps-Latscha.

At least 91 records · Page 5Linked to original sources
PubMed1989

Role of oxygen-dependent mechanisms in monoclonal-antibody-induced lysis of normal T cells by phagocytes. II. Murine phagocytes.

In the first part of this study, we reported that antibody-dependent cellular cytotoxicity (ADCC) mediated by human polymorphonuclear (PMN) and mononuclear (MN) phagocytes against anti-T-cell monoclonal-antibody-(mAb)-coated T lymphocytes, is mainly dependent upon the generation of reactive oxygen intermediates (ROI) for PMN, whereas MN-mediated ADCC depends on both oxidative and non-oxidative cytolytic events. Using mouse effector cells from various organs and at various maturation or activation states, the present report shows that in this ADCC model against mAb-coated normal T cells, resident spleen (SPC) and peritoneal exudate (PEC) cells selectively bound and developed oxidative responses to these mAb-coated normal target cells but remained ineffective in ADCC. Similar data were obtained with inflammatory recruited (thioglycollate-elicited or Biogel granuloma-induced) macrophages, whereas immunologically activated macrophages (from BCG-treated mice) mediated both strong oxidative responses and potent ADCC reactions. In contrast, and as in the human system, both resident (from bone marrow) and inflammatory PMN phagocytes exerted significant lysis of these mAb-sensitized normal lymphoid cells. These findings, which are similar to those reported in ADCC against tumour target cells, strongly suggest that the nature (normal or tumoral) of the target cell does not influence the lytic mechanisms of macrophage-mediated ADCC and that these latter require activated macrophages and, like PMN, involve strong (if not exclusive) ROI participation.

Animals↗
PubMed1988

Influence of haemodialysis membranes on beta 2-microglobulin kinetics: in vivo and in vitro studies.

Amyloidosis of the beta 2-microglobulin (beta 2M) type is a recently recognised complication of dialysis. We studied plasma and ultrafiltrate beta 2M in 36 chronic haemodialysis patients. Long-term dialysis with standard cuprophan membrane in non-oliguric patients and with the AN69 polyacrylonitrile membrane in oliguric patients resulted in lower plasma beta 2M concentrations (means +/- SD, 24.4 +/- 6.6 and 33.0 +/- 8.2 micrograms/ml, respectively) than with cuprophan in oliguric patients (47.0 +/- 13.2 micrograms/ml, P less than 0.01). In acute studies, plasma beta 2M (corrected for haemo-concentration) increased, although not significantly, during cuprophan dialysis (n = 10) from 40.6 +/- 12.2 to 44.8 +/- 7.6 micrograms/ml and decreased during AN69 dialysis (n = 10) from 39.4 +/- 18.0 to 24.3 +/- 7.1 micrograms/ml (P less than 0.02). After 15 min ultrafiltration, beta 2M sieving coefficient in vivo was 0.33 for AN69 but near zero for cuprophan. Total mass transfer of beta 2M across the AN69 membrane during a 4-h dialysis was 142 +/- 45.8 mg (n = 7). AN69, but not cuprophan, membrane fragments incubated in vitro with normal or uraemic plasma exhibited avid [125-I] beta 2M binding (respectively 12.9% vs 0.47% and 6.09% vs 0.06% of total beta 2M bound at 30 min, n = 6, P less than 0.001 for both). No in vitro generation of beta 2M from whole normal or uraemic blood could be demonstrated during incubation with either membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Macrophage oxidative activation potential in normal and endotoxin-treated Biozzi high and low antibody responder mice.

The present study is an attempt to verify the hypothesis that high (HI) and low (LI) antibody responder Biozzi mice, which differ strikingly in their macrophage capacities to catabolize antigens and to exert bactericidal activity (the LI being more potent than the HI line), demonstrate a similar genetic disparity in their macrophage oxidative metabolism activation potential. The production of reactive oxygen intermediates was measured by luminol-dependent chemiluminescence in cell suspensions from various sources including: bone marrow, peripheral blood, spleen, peritoneal exudate, thymus, and mesenteric lymph nodes. Chemiluminescence was determined both in the absence and presence of particulate (opsonized zymosan and latex) and soluble (phorbol myristate acetate and concanavalin A) membrane-stimulating agents. Lastly this investigation was conducted both in normal and endotoxin (lipopolysaccharide from Escherichia coli) treated HI and LI mice in an attempt to unmask the hypothesized difference by increasing the macrophage oxidative response capacity. Results obtained did not show the expected interline differences in reactive oxygen intermediate production regardless of cell origin, stimulating agent or lipopolysaccharide in vivo treatment. On the other hand, the well-documented enhancing effect of lipopolysaccharide on macrophage oxidative metabolism depended on the origin of the cell suspension. Indeed, it was not observed in bone marrow and peripheral blood from either HI or LI mice, was clearly demonstrated in the spleen and peritoneal exudate from both mouse lines, and surprisingly, in the thymus and lymph nodes from HI but not LI mice.

Animals↗
PubMed1986

Defective complement receptors (CR1 and CR3) on erythrocytes and leukocytes of factor I (C3b-inactivator) deficient patients.

In view of a possible modulation of the C3b receptor (CR1) by its ligand, we studied a situation in vivo in which C3b is constantly present in the serum, i.e. the genetic factor I-deficiency. C3b and iC3b receptors (CR1, CR3) on peripheral blood cells, were analysed in three I-deficient (I-def.) patients, from two unrelated families. CR1 and CR3 were quantified by means of monoclonal antibodies, and functionally tested (phagocytosis of sensitized sheep erythrocytes (EIgG) or rabbit erythrocytes (Er), coated with C3b, and chemiluminescence (CL) induced by serum-opsonized zymosan). Erythrocyte CR1 levels were significantly lower in I-def. patients than in normal individuals. Monocytes and polymorphonuclear neutrophils (PMN) prepared at 4 degrees C, to prevent increase of CR1 expression in vitro, expressed low CR1 numbers. Monocytes prepared at room temperature showed a defective CR1-dependent phagocytosis and an impaired CL response, although their CR1 levels were found normal in these conditions. This discrepancy was also observed on phorbol myristate acetate (PMA)-activated cells. These CR1 abnormalities are likely to result from repeated interactions of CR1 with C3b molecules, which circulated in the serum of I-def. patients and were deposited onto their red cells. Although iC3b, the CR3 ligand, is not produced in I-deficient sera, monocyte CR3-dependent function (phagocytosis of unopsonized Er) was also found to be defective in two out of the three patients.

Child↗
PubMed1985

Chemiluminescence monitoring of phagocyte oxidative metabolism in mice bearing polyacrylamide induced granulomas.

A technical protocol was recently described by Fauve et al. (J. Immunol. Methods 1983, 64, 345) for inducing subcutaneous granuloma with polyacrylamide microbeads. The present study using this technique demonstrates that the capacity of host phagocytes to generate reactive oxygen species can be easily monitored by chemiluminescence, both locally in granuloma infiltrating cells and at sites remote from the inflammatory reaction, i.e., within microamounts of whole blood and in spleen cells. We observed that both resting and stimulated (zymosan or phorbol-myristate acetate) production by C57BL/6 mouse phagocytes are significantly higher in granulomas induced with high porosity polyacrylamide beads (P300) than in those induced with beads of low polyacrylamide porosity (P4). Since this selective modulation of phagocyte oxidative metabolism is also detectable within microamounts of whole blood and in spleen cells, it could serve as a model for investigating the role of reactive oxygen species in the inflammatory reaction.

Acrylic Resins↗
PubMed1985

Hemodialysis membrane-induced activation of phagocyte oxidative metabolism detected in vivo and in vitro within microamounts of whole blood.

The production of reactive oxygen species by phagocytes from uremic patients undergoing hemodialysis was monitored by chemiluminescence (CL) within microamounts of whole blood or isolated polymorphonuclear (PMN) cells, and compared on the basis of the dialysis membrane, cuprophane (CUP) or polyacrilonitrile (PAN). Compared to control subjects, resting and stimulated CL (with latex, zymosan, phorbol myristate acetate (PMA) but not formyl-methionyl-leucyl-phenylalanine (FMLP) were decreased in 10(-2) diluted blood sampled before dialysis. After 15 min of dialysis (ti), resting whole blood (10(-1) and 10(-2) diluted) CL increased sharply in patients dialyzed with the CUP but not the PAN membrane, while it returned to its predialysis level at the end of the session. This sharp resting CL increase found in whole blood at ti was not observed in isolated PMN cells except when tested with ti plasma from CUP dialyzed patients, suggesting that it was mediated via activated plasma compounds. In vitro treatment of normal blood, plasma, and isolated PMN cells with CUP membrane fragments reproduced this in vivo dialysis-induced activation of phagocyte oxidative metabolism strikingly and demonstrated additionally the requirement of complement for its induction. We propose this model as an effective means of evaluating dialysis membrane biocompatibility.

Acrylic Resins↗
PubMed1985

Altered oxidative metabolism, motility, and adherence in phagocytic cells from cystinotic children.

The present study investigates whether the metabolic abnormalities in cystinotic cells could affect nonspecific immune responses. Lymphocytes showed normal antibody-dependent cellular cytotoxicity and natural killer activity. However, cystinotic polymorphonuclear and mononuclear phagocytes exhibited altered oxidative responses as monitored by a luminol dependent chemiluminescence (CL) assay. Both isolated polymorphonuclear and mononuclear phagocytes in the absence of stimuli showed significantly increased CL production which was not found when cells were tested directly within whole blood. CL responses to a panel of stimuli differed markedly according to the type of cells and agents tested. Indeed, isolated polymorphonuclear demonstrated increased CL responses to soluble but not particulate agents, whereas isolated mononuclear phagocytes and overall cell CL responses in whole blood were found to be within the normal range regardless of the type of stimulus used. We also studied some membrane related properties of phagocytic cells. Fc and C3b receptors were normally expressed as tested by erythrocyte-antibody and erythrocyte-antibody-complement rosette-forming cells. Nevertheless, cystinotic polymorphonuclear and mononuclear phagocytes presented decreased random and directed migrations in an under-agarose chemotaxis assay. Finally, cystinotic granulocytes showed an impaired adhesiveness in a nylon fiber assay.

Cell Adhesion↗
PubMed1985

Deleterious effects of cardiopulmonary bypass. A prospective study of bubble versus membrane oxygenation.

A number of hematologic and immunologic parameters that reflect erythrocyte and platelet damage and host defense mechanisms against infection were studied in 20 patients undergoing cardiopulmonary bypass during coronary operations. The patients were randomly assigned to a group in which a bubble oxygenator or a hollow-fiber membrane oxygenator was used. Hemolysis, thrombocytopenia, and significant release of beta thromboglobulin occurred in patients from the bubble oxygenator group and, to much lesser extent, in patients from the membrane oxygenator group. Polymorphonuclear leukocytes and monocytes from bubble oxygenator patients demonstrated increased generation of reactive oxygen species in the resting state and in the presence of the stimulating agents N-formyl-methionyl-leucyl-phenylalanine, concanavalin A, and opsonized zymosan, as compared with cells from membrane oxygenator patients. No difference was found between bubble and membrane oxygenator patients in the time of occurrence or intensity of leukopenia during bypass, of leukocytosis at the end of bypass, nor in the rate of complement activation, as assessed by quantitation of plasma C3a antigen. Complement activation was dependent on the alternative pathway. Immunoglobulin M concentration significantly decreased during bypass in both groups of patients. The serum opsonizing capacity for endotoxin and serum bactericidal activity for Serratia marcescens were decreased in both groups, mainly because of hemodilution, although they were additionally affected by bubble oxygenation. Several deleterious hematologic consequences of cardiopulmonary bypass can be minimized by the use of a membrane oxygenator. However, complement activation remains a potential risk factor even in membrane oxygenator patients and requires further investigation to obtain better hemocompatible materials for cardiopulmonary bypass circuits.

Blood Bactericidal Activity↗
PubMed1984

[Activation of oxidative metabolism of granulocytes and monocytes by IGG-coated platelets from patients with thrombocytopenia].

We have previously shown that monoclonal anti-T cell antibodies bound to their specific targets can trigger the activation of monocyte/macrophage oxidative metabolism through an Fc receptor-mediated interaction. The present study demonstrates that IgG coated platelets from patients with thrombocytopenia-associated diseases can induce a similar respiratory burst activation in polymorphonuclear and mononuclear phagocytes from normal individuals. The intensity of the oxidative reaction as measured by luminol-dependent chemiluminescence is in close correlation with the level of surface-bound IgG molecules as determined by a radioactive anti-immunoglobulin assay. This new methodology to evaluating IgG fixed on human platelets by their capacity to trigger the generation of highly reactive oxygen species by granulocytes and monocytes has also suggested a new mechanism in the genesis of thrombocytopenia associated with autoimmune diseases.

Cell Membrane↗
PubMed1984

Effect of LPS on the oxidative metabolism of peritoneal and spleen cells from LPS sensitive and resistant mice.

The influence of LPS on peritoneal and spleen cell oxidative metabolism was investigated in LPS sensitive (C57BL/6) and LPS resistant (C3H/HeJ) mice following intraperitoneal or subcutaneous injection, by measurement of chemiluminescent (CL) responses to latex particles. In C57BL/6 mice, LPS induced a marked increase in peritoneal and spleen cell CL responses, regardless of the route of injection. On the 2nd day, the effect of LPS on peritoneal cells could be fully explained by an inflammatory reaction, while on the 4th day it could be related to an "activated state" of peritoneal macrophages. In contrast, such an in vivo effect of LPS in peritoneal or spleen cell CL responses was not found in C3H/HeJ mice except on the 2nd day following the injection and with the highest LPS dosage and could be totally due to the LPS induced inflammatory reaction. In vitro studies showed that extremely low concentration of LPS increased CL response capacities of C57BL/6 spleen cell to latex particles. In contrast, CL responses from C3H/HeJ spleen cells remained unaffected by LPS except when submitted to concentrations which proved toxic for the sensitive strain CL producing cells. These results lend additional evidence for the involvement of reactive oxygen species (ROS) in the metabolic consequences of LPS-induced macrophage activation.

Animals↗
PubMed1983

Bone-marrow transplantation for inborn error of phagocytic cells associated with defective adherence, chemotaxis, and oxidative response during opsonised particle phagocytosis.

Two girls had delayed umbilical cord detachment, recurrent bacterial infection, inability to form pus, and marked leucocytosis. Their phagocytes were defective in tests of adherence, random migration, chemotaxis, and oxidative burst. NK activity was virtually absent. This rare disorder, due to an inherited absence of a 180 kilodalton membrane glycoprotein on polymorphonuclear cells, is usually lethal within 2 years. Allogeneic HLA-matched bone-marrow transplantation done at ages 4 months in one patient and 2 years in the other after intensive conditioning was successful and resulted in nearly complete correction of phagocytic cell function and NK activity within two months. One patient died 9 months after transplantation from severe chronic graft-versus-host disease with obstructive bronchopneumopathy. The other is doing well 1 year after transplantation and showing stable chimerism and normal phagocytic function.

Bone Marrow Transplantation↗
PubMed1983

Monoclonal antibodies against T cell differentiation antigens initiate stimulation of monocyte/macrophage oxidative metabolism.

Within the first minute after incubation with the mouse anti-human T cell orthoclone monoclonal antibodies OKT3, OKT4, and OKT8, and in the absence of complement, human monocytes generate a burst of highly reactive oxygen metabolites as detected by a luminol-dependent photometric chemiluminescence (CL) assay. The kinetics of the CL responses to these antibodies are identical to that induced by OKM1, the monoclonal antibody to human monocytes and granulocytes. With regard to CL response intensities, OKM1 induces the maximal response and those of OKT3, OKT4, and OKT8 closely reflect the proportion of T cell subsets recognized by these antibodies in peripheral blood. This reaction is also observed when monoclonal antibodies against mouse Lyt surface determinants (Lyt-1 and Lyt-2) and Thy-1 antigen are tested against murine spleen cells. This murine model was further used to investigate the specificity and the mechanism of this reaction. It was demonstrated that the CL response is Lyt antigen specific, occurs upon addition of monoclonal IgG but not IgM antibodies, requires the concomitant presence of CL-producing cells (CLPC) (promonocytes, monocytes, macrophages, and/or granulocytes) and of fully differentiated T cells, and lastly, is mediated via a T cell opsonization process. Selective blockade of bone marrow cell Fc receptors (FcR II) with monoclonal anti-mouse FcR II antibody inhibits the CL response to IgG2b anti-T cell antibody-coated thymocytes and thus strongly suggests that the stimulation of CLPC oxidative metabolism in this model results from the binding of opsonized T cells to plasma membrane Fc receptors. These observations lend additional support to increasing evidence that the initiation of effector functions by monoclonal anti-T cell antibodies may be strictly dependent upon the presence of monocytes and/or macrophages.

Animals↗