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F Peyron

Publications and source records attributed to F Peyron.

At least 19 recordsLinked to original sources
PubMed1992

Monocyte tissue factor expression induced by Plasmodium falciparum-infected erythrocytes.

Monocytes are active elements of the host response against Plasmodium falciparum. They are able to express tissue factor and trigger the extrinsic pathway of blood coagulation the activation of which remained unclear in malaria. Our aim was to assess the tissue factor expression of purified blood monocytes stimulated by cultured Plasmodium falciparum-infected erythrocytes. Malaria parasite induced an early generation of tissue factor with a peak between 8 and 12 h of stimulation. Maximum expression was observed for parasitemia ranging from 1 to 2%. Plasmodium falciparum culture supernatants had the same effect showing the existence of a soluble factor able to induce the tissue factor expression. These data, demonstrating an activation of the tissue factor pathway by the malaria parasite, emphasize thrombin generation. Therefore, thrombin could participate in malaria pathology either in the microcirculatory blockade via platelet and fibrinogen activation or as a mitotic.

Animals↗
PubMed1992

Relationships between circulating S-antigens, naturally acquired antibodies to Plasmodium falciparum exoantigens and malaria attack in a mesoendemic area.

A survey involving 77 individuals living in two savannah villages near Bobo Dioulasso (Burkina Faso, West Africa), was performed in June 1987 (before), August-September (during) and January 1988 after the seasonal transmission. The clinical longitudinal study during the seasonal period permitted us to define three different groups in terms of both age and occurrence of malaria attack (MA; greater than or equal to 5000 parasites/mm3 of blood and axillary fever greater than or equal to 37.8 degrees C). The presence of circulating stable antigen (S-Ag) and the antibody responses against exoantigens (E-Ag) of Plasmodium falciparum were also evaluated at three observations periods: beginning, during and after the transmission season. The adult group (III) had the highest rates of IgG Ab to E-Ag although, IgM prevalence to E-Ag was maximal in the group II (individuals with no malaria attack and age less than or equal to 15 years old). Group I (persons with less than or equal to 15 years old and who contracted at least one MA) did not have any S-Ag at the first observation period and showed the lowest rate of antibodies to E-Ag. The probability of occurrence of an MA calculated from these parameters at the beginning of the transmission period were correct in 78.9% of the cases in children (Groups I & II) and in 71.8% of adults during the subsequent transmission period. Therefore these values could be used for evaluating the probability of occurrence of a clinical MA during the transmission period in a mesoendemic area. S-Ag and antibodies to E-Ag could participate positively in the mechanisms involved in the development of the immune status.

Adolescent↗
PubMed1992

Rapid in vivo detection of chloroquine resistance by the Quantitative Buffy Coat Malaria Diagnosis System.

The use of the Giemsa-stained thick blood smear for the diagnosis of malaria has not been supplanted since the discovery of the parasite by A. Laveran in 1880. Recently, a new direct diagnosis technique, the Quantitative Buffy Coat (QBC)* Malaria Diagnosis System, has been developed. We compared this technique with the thick blood smear diagnosis in a study of the efficacy of chloroquine therapy in Zaire. A total of 815 subjects were screened; 71 participated in the trial. They were given chloroquine at a dose of 25 mg/kg of body weight over three days and were examined for parasitemia two and seven days after treatment. Chloroquine resistance was detected in 38% of the subjects by thick blood smear and in 45% by the QBC test. Of greater interest was the time required for each diagnosis: an average of 17 min was required to examine microscopic fields with 1,000 leukocytes by thick blood smear analysis compared with less than one min by the QBC system. In addition, we did not observe diminished attention from fatigue by microscopists using the QBC system despite the large number of tests conducted. We conclude that the QBC system is an important tool for studies of drug resistance.

Animals↗
PubMed1991

Relationships between clinical protection and antibodies to Plasmodium falciparum RESA (ring-infected erythrocyte surface antigen) peptides.

A longitudinal study involving 76 individuals living in Dafinso and Vallée du Kou (near Bobo-Dioulasso, Burkina Faso, West Africa) was performed in June 1987 (beginning of the transmission period), August-September 1987 (during) and January 1988 (after). The serological antibody (Ab) responses against synthetic peptides representing repeat amino acid sequences of the P. falciparum Ring-Infected Erythrocyte Surface Antigen (RESA): (EENV)5, (EENVEHDA)4, (DDEHVEEPTVA)2 were evaluated by ELISA. The clinical longitudinal study during the transmission period allowed us to define three different groups in terms of age and occurrence of clinical malarial attack (greater than 5000 parasites mm-3 of blood and axillary fever greater than 37.7 degrees C). Levels (A620) of Ab to (EENVEHDA)4 and (DDEHVEEPTVA)2 were correlated with age. The adult group (III) had the highest prevalences of Ab to RESA peptides. No significant difference was found between groups of children with or without malaria attack. Nevertheless, at the beginning of the transmission period, children who had at least one malaria attack during the study presented the lowest level of antibodies to RESA peptides.

Animals↗
PubMed1991

Development of natural immunity in Plasmodium falciparum malaria: study of antibody response by Western immunoblotting.

A longitudinal study was carried out in Burkina Faso to investigate the natural development of the immune response to Plasmodium falciparum malaria. Three bleedings were carried out before, during, and after the seasonal peak of transmission. Detailed antigen mapping and antibody prevalence of the 248 collected serum samples were established by immunoblotting on the basis of several epidemiological and biological parameters. An improved Western immunoblotting system was used to analyze up to 67 serum samples on each nitrocellulose sheet. This system allowed us to perform the entire study with strictly comparable conditions. Two different blood-stage antigens (exoantigens and somatic antigens) were used to analyze the distribution of different classes and subclasses of immunoglobulins according to the age of the individuals, the presence or absence of a malarial attack, the transmission period, the origin of parasite isolates, and the response to intraerythrocytic stages. Although this analysis emphasizes strong individual variations, reactions with two major antigens of 115 and 103 kDa were especially noted. These antigens induced high antibody levels and prevalences but were probably not involved in protection. The prevalence of immunoglobulin G (IgG) antibodies differed by isotype. Most of antigens stimulating IgG production were also responsible for the IgM antibody response. The role played by these antibodies in the development of natural immunity against malaria is discussed.

Adolescent↗
PubMed1991

Levels of cytokines in plasma during Plasmodium falciparum malaria attacks.

The variation of levels of tumor necrosis factor, granulocyte-macrophage colony-stimulating factor, gamma interferon, neopterin, and interleukin-2 receptors in plasma were monitored in 16 patients presenting with an acute Plasmodium falciparum malaria attack. Relations among cytokine levels and between cytokine levels and hematological and parasitological data were assessed.

Adult↗
PubMed1991

Platelet cytotoxicity against parasites.

Platelets are not restricted to hemostasis and thrombosis since they are involved in defence mechanisms especially in parasitic diseases. They express cytotoxic functions in vitro and in vivo against extra-cellular and intra-cellular parasites. The toxic process is mediated either by specific antibodies or directly by the parasite itself. As some metabolic pathways seem to be implicated both in hemostasis and in parasiticidal activity, primary hemostasis and cytotoxicity may be considered as specialized inflammatory responses.

Animals↗
PubMed1991

[Tumor necrosis factor during the course of neuromalaria: new therapeutic perspectives].

Malaria remains one of the major public health problem in tropical and subtropical world. Malaria pathogeny depends partly on parasite multiplication and partly on some elements of the immunological response. It has recently become evident that one of these elements, Tumor Necrosis Factor (TNF), is directly implicated in the pathogenesis of cerebral malaria. TNF increase cytoadherence of infected erythrocytes to the brain microvascular endothelium. In a study involving african children with cerebral malaria high levels of TNF were positively correlated with a fatal outcome. We have previously demonstrated that in vitro Plasmodium falciparum products can directly stimulate the production of TNF from human macrophages. The aim of this work was to identify this soluble parasitic substance. Our results demonstrated that this substance could be a repetitive amino-acid sequence of the Ring-infected Erythrocyte Surface Antigen (RESA). The immunization against this kind of well-known peptides may be used as anti-disease vaccine. The elimination of mortality would be an essential target instead of parasitic clearance.

Antigens, Protozoan↗
PubMed1990

Plasma levels of tumor necrosis factor during a longitudinal survey in an endemic area of malaria.

The plasma levels of tumor necrosis factor were measured during a longitudinal survey of 84 subjects living in an endemic area of malaria. In most cases, the plasma tumor necrosis factor was found at its highest level during the malaria transmission peak and became normal again during the dry season. Children having suffered from malarial attack keep low tumor necrosis factor levels compared to adults and asymptomatic children. These results suggest that tumor necrosis factor could be associated with the development of resistance against malaria.

Adolescent↗
PubMed1990

Correlation between beta 2-microglobulin and soluble interleukin-2 receptor levels in plasma of individuals living in a malarial endemic region.

beta 2-Microglobulin (beta 2m) levels were related to the expected immunoprotection in 81 individuals living in a malarial mesoendemic area near Bobo-Dioulasso (Burkina Faso), who were longitudinally followed. Soluble interleukin-2 receptor (sIL-2R) levels were positively correlated to those of beta 2m (r = 0.44; n = 237; P less than 0.001). This suggests that most of the beta 2m could have originated from activated T and B cell membrane turnover. In our study, both beta 2m and sIL-2R were inversely related to IgG antibodies (Ab) against somatic antigen of Plasmodium falciparum (Som-Ag). Therefore, these molecules at high levels could have a down regulating activity, directly or indirectly, on B cells producing this kind of Ab.

Adolescent↗
PubMed1990

Tumor necrosis factor production by human macrophages stimulated in vitro by Plasmodium falciparum.

Production of tumor necrosis factor by human macrophages may be induced in vitro by cytoadherent and noncytoadherent strains of Plasmodium falciparum, with an optimal ratio of one to three parasitized erythrocytes per macrophage. Centrifuged and heated crude culture supernatants have the same effect, thus showing the existence of a thermostable soluble factor able to induce this expression. In vitro kinetic experiments have shown that the secretion of tumor necrosis factor appears early, with a maximal peak at 8 h.

Animals↗
PubMed1990

Longitudinal survey in an endemic region of plasma soluble interleukin-2 receptor and antibody levels in Plasmodium falciparum malaria.

A survey involving 81 individuals living in Dafinso and Vallée du Kou no. 4 (near Bobo-Dioulasso), Burkina Faso, was performed in June 1987, August to September 1987, and January 1988, respectively, at the beginning of, during, and after the transmission season of malaria. The clinical longitudinal study during the transmission period allowed us to define three different groups in terms of both age and occurrence of malaria attack (5,000 Plasmodium falciparum per mm3 of blood and axillary fever of greater than 37.7 degrees C) as follows: group 1, persons less than or equal to 15 years old who had at least one malaria attack during the transmission period; group 2, individuals less than or equal to 15 years old who did not have any malaria attacks; and group 3, individuals considered to be protected (adults greater than 15 years old with no malaria attacks). Soluble interleukin-2 receptor (sIL-2R) levels were found to be significantly increased (P less than 0.001) in the first two groups (1,047 +/- 481 U/ml [mean +/- standard deviation]) as compared with the adult group (605 +/- 307 U/ml). Considering all the groups, no significant difference was observed between observation periods. Levels of sIL-2R were inversely correlated (r = -0.39, n = 237, P less than 0.01) with age (range, 4 to 67 years). Negative correlations were also noticed between the levels of sIL-2R and those of antibodies to somatic antigen of P. falciparum (immunoglobulin G [IgG] class [r = -0.33, n = 237, P less than 0.01] and IgM class [r = -0.20, n = 237, P less than 0.05]). IgG antibody levels to somatic antigen were correlated with age, but IgM antibody levels to somatic antigen were not. The possible role played by sIL-2R in effector mechanisms against malaria is discussed.

Adolescent↗
PubMed1990

[Erythrocytes infected by Plasmodium falciparum activate human platelets].

Blood platelets are involved in Plasmodium falciparum malaria pathology as shown by thrombocytopenia and increased plasma level of two alpha granule proteins: beta thromboglobulin (beta TG) and platelet factor 4 (PF4). In this study we demonstrate that Plasmodium falciparum parasitized erythrocytes activate directly the secretion of beta TG and PF4 by human platelets. This secretion is related to parasitemia and occurs immediately after contact. Treatment of parasited erythrocytes by trypsin and diffusion chamber experiments suggest that platelet activation is triggered by parasitic substances shed on erythrocyte membrane and released in the culture medium.

Animals↗