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J L Mege

Publications and source records attributed to J L Mege.

83 records · Page 5Linked to original sources
PubMed1986

Self-limitation of the oxidative burst of rat polymorphonuclear leukocytes.

The oxidative response of rat polymorphonuclear leukocytes stimulated by phorbol myristate acetate and N-formyl-methionyl-leucyl-phenylalanine was studied. Ferricytochrome reduction and peroxidase-catalyzed decrease of scopoletin fluorescence were used to monitor O-2 and H2O2 release in the extracellular medium. Oxygen consumption was also measured in some experiments. Decrease of chlortetracyclin fluorescence after stimulation of dye-loaded cells was used to study an early step of cell stimulation. Finally, a possible relationship between cell responses and the medium redox potential was explored. Three major conclusions were obtained: Ferricytochrome reduction is dependent on the total cytochrome concentration, and a simple mathematical model allows a tentative estimate of total superoxide anion production by stimulated cells. Increasing cell concentration results in a decrease of individual cell response, and this may be accounted for by a direct inhibition of cell-released hydrogen peroxide on the reactivity of leukocytes. Further, H2O2 may be shown to inhibit an early step of cell response. The solution redox potential does not influence cell reactivity, since it may be dramatically decreased without inhibiting cell response.

Animals↗
PubMed1986

Determination of binding strength and kinetics of binding initiation. A model study made on the adhesive properties of P388D1 macrophage-like cells.

The adhesive properties of the mouse P388D1 macrophage-like line were explored. Cells were deposited in glass capillary tubes, and the kinetics of adhesion and spreading were studied. Binding involved the cell metabolism since it was decreased by cold, azide, or a divalent cation chelator. Glass-adherent cells were subjected to calibrated laminar shear flows with a highly viscous dextran solution. A tangential force of about 5 X 10(-3) dyn/cell was required to achieve substantial detachment. The duration of application of the shearing force strongly influenced cell-substrate separation when this was varied from 1-10 s. Further, this treatment resulted in marked cell deformation, with the appearance of an elongated shape. Hence, cell-substrate separation is a progressive process, and binding strength is expected to be influenced by cell deformability. The minimum time required for adhesion was also investigated by making cells adhere under flow conditions. The maximum flow rate compatible with adhesion was about 1000-fold lower than that required to detach glass-bound cells. A simple model was devised to provide a quantitative interpretation for the experimental results of kinetic studies. It is concluded that cell-to-glass adhesion required a cell-substrate contact longer than a few seconds. This first step of adhesion was rapidly followed by a large (about 1000-fold) increase of adhesion strength. It is therefore emphasized that adhesion is heavily dependent on the duration of cell-to-cell encounter, as well as the force used to remove so-called unbound cells.

Animals↗
PubMed1986

[Role of phagocytic cells in rheumatoid polyarthritis].

Three groups of subjects were selected for this study. Patients suffering from rheumatoid arthritis (RA) diagnosed according to the criteria of the ARA (mean: 6 criteria) and treated with gold salts. Control subjects treated with one type of non-steroidal anti-inflammatory agent (diclofenac). Healthy subjects receiving no treatment. The granulocytes and monocytes in the peripheral blood were tested separately for the ingestion of 3 types of particles and for the stimulation of the production of the superoxide anion. In the patients with rheumatoid arthritis, all of the phagocytic cells had a normal phagocytic response and a normal superoxide anion production. The serum of the patients did not inhibit the activity of these cells. Diclofenac did not act on phagocytosis or on the oxidative activity of the control cells. It is therefore logical to consider that the phagocytic cells are involved in RA via other mechanisms of action.

Adolescent↗
PubMed1985

Study of cell deformability by a simple method.

Cell deformability plays an important role in many immunological processes, such as phagocyte chemotaxis and endocytosis. The most widely used method of assay consists in aspirating cells into glass micropipettes and measuring the length of the protrusion induced by a given pressure, or the minimum pressure required to drive cells into the micropipette. This procedure requires specialized equipment and delicate manipulation. The present report describes a simpler procedure: cells are centrifuged in petri dishes floating on a water cushion, then fixed and coated with 0.8 micron diameter latex beads, which allows rapid and accurate determination of their height. This method is compared with the micropipette technique by studying lymphocyte and macrophage-like cell lines in physiological medium and in the presence of a divalent cation chelator or a microfilament inhibitor. In addition to simplicity, the main advantages of this technique are that (i) many cells may be examined within a reasonable period of time, which allows testing of heterogeneous cell populations, and (ii) unexpectedly, centrifugation was quite harmless under our experimental conditions, since it did not impair cell proliferative ability nor phagocytic ability. It is concluded that the method may be used in clinical laboratories to explore phagocyte dysfunctions, as well as in experimental studies.

Animals↗
PubMed1985

Monocytes and granulocytes in rheumatoid arthritis (RA): phagocytic activity and superoxide anion production.

It is suggested by many tests that phagocytic cells were implied in inflammation which occurred during rheumatoid arthritis (RA). Further, three subject populations were selected for this study: Rheumatoid arthritis patients diagnosed according to American Rheumatism Association criteria (ARA mean = 6) and treated with gold compounds. Control subjects treated with the same non-steroidal anti-inflammatory drug (NSAID), diclofenac (75 mg per day). Normal subjects without disease or treatment. Blood granulocytes and monocytes were separately tested for ingestion of three different particle species (opsonized zymosan, immunoglobulin G sheep red cells, glutaraldehyde-treated sheep red cells) and stimulation of superoxide anion production by these particles. All phagocytic cells in RA patients have normal phagocytic response and superoxide anion production. Autologous serum does not inhibit the activity of these cells. In addition the NSAID (diclofenac) does not act upon phagocytosis and oxidative burst of control cells.

Adolescent↗
PubMed1984

Nonspecific cell surface properties: contact angle of water on dried cell monolayers.

Measuring contact angle of water on dried cell or bacterium monolayers allowed van Oss (1) and others (2) to find a correlation between particle hydrophobicity and ingestion by phagocytic cells. The present study was undertaken to understand what was actually assayed with this method. Monolayers were prepared with different cell types at different densities, and they were dried under atmospheres with varying humidity before being studied with scanning electron microscopy and contact angle techniques. It is concluded that a) contact angles are independent of the cell density and substrate structure when more than 30% of the substrate area is covered with cells. b) Initial cell shape should not influence contact angle. c) Contact angles are markedly dependent on the nature of tested cells. d) Contact angles are substantially influenced by the cell drying procedure. e) A very small fraction of the energies we measured would be sufficient to account for cell-cell interactions. Hence these might play a role in some situations of biological interest.

Animals↗
PubMedDate not supplied

Protein tyrosine kinases and TNF alpha secretion in human monocytes.

The role of protein tyrosine kinases (PTK) in TNF alpha secretion by human monocytes was investigated in this report. We showed that an immunomodulator such as Nocardia lysozyme digest (NLD) and a particulate agonist, zymosan, stimulated an increase in tyrosine phosphorylation of several endogenous substrates including 53-56 kDa protein which was the predominant phosphoprotein. In addition, NLD and zymosan induced TNF alpha secretion which was impaired by a PTK inhibitor, tyrphostin. We suggest that a cascade of kinases including PTK is involved in NLD and zymosan signalling.

Humans↗
PubMedDate not supplied

Phagocytic cell function in aged subjects.

In order to study the activity of phagocytic cells in normal and pathological aging, we compared normal young and aged subjects and patients with Alzheimer's (AD) or Parkinson's (PD) disease. Blood granulocytes and monocytes were separately assayed for ingestion of three different particle species (opsonized zymosan, immunoglobulin-coated sheep red cells (IgG-SRC) and glutaraldehyde-treated sheep red cells (G-SRC]. The superoxide anion production induced by these particles was also measured. All granulocyte responses to zymosan and IgG-SRC were depressed in the three aged groups as compared to young controls. Hence, only functions involving a specific receptor (Fc or C3b receptor) seemed affected. Monocyte activity was slightly decreased in the same groups. No difference was found between AD or PD patients and normal aged subjects. Hence the phagocytic and oxidative defects we found were a consequence of aging.

Adult↗
PubMedDate not supplied

Effect of botulinum D toxin on human neutrophilic leukocytes and localization of its substrates.

Botulinum D toxin has been shown to ADP-ribosylate 22-kD proteins in neutrophilic leukocytes, but the function of these GTP-binding proteins remains unknown. In analogy to small GTP-binding proteins like SEC4 to YPT1, it has been suggested that botulinum D toxin substrates might be involved in secretory process of myeloid cells. Three main findings lead to the opposite conclusion. First of all, in human neutrophils, botulinum D toxin does not modify the release of azurophilic and specific granules induced by a chemoattractant (a formylpeptide) or a phorbol ester. Second, botulinum D toxin ADP-ribosylates 24 to 26-kD proteins that are only present in plasma membranes of human neutrophils. The membrane location of these substrates differs largely from that of the GTP-binding proteins involved in exocytosis and located in granules. Finally, since the same quantity of the toxin substrates is present in neutrophils as in their precursors, HL60 cells (which are devoid of specific granules and characterized by immature azurophilic granules and NADPH oxidase), it is unlikely that endogenous botulinum D toxin substrates are directly involved in the secretory responses of neutrophils.

Botulinum Toxins↗