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Biomedical subjects

H Watier

Publications and source records attributed to H Watier.

29 records · Page 2Linked to original sources
PubMed1995

Tissue factor activity of syncytiotrophoblast plasma membranes and tumoral trophoblast cells in culture.

During pregnancy, important modifications of hemostasis occur resulting in mothers in hypercoagulability and the role of placental cells such as trophoblast cells has been hypothesized. In this study, we first showed that syncytiotrophoblast plasma membranes, isolated from normal human placenta, expressed a strong tissue factor (TF) activity. We then studied TF activity of two continuous trophoblast cell lines (JEG-3 and BeWo) in comparison to human umbilical vein endothelial cells (HUVEC) and transformed human endothelial cells (ECV-304). TF assays were performed on intact detached confluent cells. Unstimulated JEG-3 and BeWo cells exhibited a very high TF activity which slightly increased after 2 to 4 h TNF-alpha stimulation. In contrast, HUVEC and ECV-304 had a lower basal TF activity which was mainly inducible by TNF-alpha, with a maximum effect after 4 to 6 h stimulation. For both cell types, TF activity was decreased to basal value after 16-hour TNF-alpha stimulation. These results support that trophoblast cells are able to express TF but the involvement of this property in the hemostatic physiological changes observed during pregnancy, remains to be demonstrated.

Cell Line, Transformed↗
PubMed1994

Adhesive properties of choriocarcinoma cells toward lymphocytes activated or not by interleukin-2.

Choriocarcinoma cells (CC) in vitro are resistant to NK lysis but sensitive to lysis by blood or decidual effectors activated by interleukin-2 (IL-2). Because lytic activity requires a step of adhesion, the adhesive properties of the choriocarcinoma cells BeWo, JEG-3, and JAR were examined functionally toward peripheral blood lymphocytes. The adhesion of lymphocytes to choriocarcinoma cells was very low and did not increase after stimulating lymphocytes with IL-2. As demonstrated by cytofluorimetry analysis, choriocarcinoma cells and cytotrophoblast cells prepared from term placenta expressed intercellular adhesion molecule-1 (ICAM-1), whereas only CC expressed CD56. Tumor necrosis factor-alpha or interferon-gamma increased the expression of ICAM-1 on choriocarcinoma cells without modifying the adhesion of lymphocytes to choriocarcinoma cells. These results suggest that resistance of choriocarcinoma cells to lysis by cytotoxic effectors could partially be attributed to the low level of lymphocyte adhesion to these cells.

Cell Adhesion↗
PubMed1993

IFN-gamma treatment of rodents infected with erythrocytic stages of Plasmodium chabaudi: differential effects according to the immunological status.

Recombinant rat interferon-gamma (rrIFN-gamma) was tested for its antimalarial activity in three different models of Plasmodium chabaudi-blood stage malaria. Doses ranging from 1 x 10(4) to 1 x 10(5) U of rrIFN-gamma were used in each model. In BALB/c mice (lethal infection), prophylactic treatment with daily intraperitoneal (i.p.) injections reduced parasitemia and delayed mortality. In contrast, subcutaneous administration of rrIFN-gamma was inefficient, as was curative schedule of i.p. administration. Euthymic Fischer rats, which develop an acute and resolutive infection, were partly protected by i.p. prophylactic administration of rrIFN-gamma. Parasitemia was reduced without being lengthened, resulting in a marked decrease in parasite burden. Subcutaneous administration was less efficient whereas curative schedule was not. Athymic (nude) Fischer rats which present a longlasting and stable infection were treated with prophylactic and curative schedules of i.p. administration of rrIFN-gamma. In each case, rrIFN-gamma-treated nude rats, as control nude rats, were unable to resolve their chronic infection. The conditions required to obtain a beneficial effect are thus restrictive for a therapeutic use in humans. Moreover, these results show that, despite the fact that IFN-gamma is considered as a major component of the immune response, this cytokine alone is not sufficient to induce the totality of the effector mechanisms necessary to cure malarial infections.

Animals↗
PubMed1992

T-cell-dependent immunity and thrombocytopenia in rats infected with Plasmodium chabaudi.

Normal, splenectomized, and athymic Fischer rats were infected with Plasmodium chabaudi. In normal rat infections, acute-phase infection resolved rapidly and completely. In splenectomized rats, infection resulted in high parasitemia and ultimately death. In nude rats, parasite growth was reduced compared with normal rats, and a persistent parasitemia (between 20 and 45%) was observed for several months. Complete resolution of the infection was achieved after adoptive transfer of T lymphocytes, even when transfer occurred during the course of infection. These results indicated that an acquired, T-lymphocyte-dependent immunity was necessary for the complete recovery observed in normal rats. In normal rats, thrombocytopenia and splenomegaly occurred during infection. By contrast, in nude rats, both of these pathological manifestations were only observed after thymus grafting. Thrombocytopenia was also absent in the splenectomized animals. Despite an increase in platelet-associated immunoglobulin levels during the infection, thrombocytopenia was not transferred by injection of infected rat serum to normal recipients. It has been concluded that the nude rat infection can be regarded as a novel and useful model for studying the T-cell-dependent effector and pathological mechanisms and to investigate the anti-P. chabaudi immune response.

Animals↗
PubMed1991

ELISA for the detection of anticardiolipin antibodies. High specificity based on the use of adult bovine serum as buffer and systematic subtraction of non-specific binding.

We have used an ELISA procedure to compare the reactivity of samples with or without IgG anticardiolipin antibodies (ACA) on cardiolipin-coated wells (target wells) and cardiolipin-free wells (control wells), using 10% fetal calf serum (10% FCS), 10% adult bovine serum (10% ABS) or 1% bovine serum albumin (1% BSA) as buffer. With 1% BSA, ACA reactivity was very low which suggests that this buffer would be inappropriate for use in ELISA procedures for ACA. 10% FCS induced non-specific binding of normal IgG only on target wells, particularly in the case of IgG hypergammaglobulinemia. With 10% ABS, this non-specific binding occurred on the solid phase with and without cardiolipin and could be accurately evaluated by subtracting the absorbance of control wells. Results of assays on 35 systemic lupus erythematosus sera using 10% ABS as buffer showed that highly specific results-could be obtained only if non-specific binding was systematically subtracted.

Adult↗
PubMedDate not supplied

Effect of rIFN-gamma and IL-2 treatments in mouse and nude rat infections with Toxoplasma gondii.

Mice and nude rats lethally infected with T. gondii and treated with recombinant rat interferon-gamma (rIFN-gamma) or recombinant human interleukin-2 (rIL-2) were protected against death, when compared with untreated infected controls. In mice rIFN-gamma and rIL-2 played an important role in "prophylactic treatment", but not in "curative therapy". The survival rate was 42% in mice treated with 3 doses of 20,000 U of rIFN-gamma at days -2, -1, 0 before challenge and up to 66% in mice treated with 3 doses of 10,000 U of rIFN-gamma at days -2, 0, +2 before and after infection. Whereas the survival rate was 33% in mice that received 3 doses of 500 U rIL-2 at days -2, -1, 0 before infection, or -2, 0, +2 before and after infection respectively, up to 50% of the mice treated with 3 doses of 1,000 U rIL-2 at days -2, -1, 0 survived. In nude rats rIFN-gamma had a slight effect in "prophylactic treatment", whereas rIL-2 was active only in "curative treatment". The survival rate was 25% both in nude rats treated with doses of 400,000 U of rIFN-gamma at days -3, 0 before challenge, or with doses of 5,000 U of rIL-2 at days +2, +6, +9 after infection. These results lead us to hypothesise that the mechanism by which the lymphokine treatment exerts a protective effect on Toxoplasma infected mice is different from that on nu/nu rats. We conclude that these cytokines may play a notable role in modulating the host's immune defence against T. gondii infection.

Animals↗