60 results on '"Bonnefoy, Serge"'
Search Results
52. PFHRP2 PERSISTENCE IN 'ONCE INFECTED RBC' ENABLES A RAPID PREDICTION OF POST-ARTESUNATE DELAYED HEMOLYSIS
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Ndour, Papa Alioune, Larreche, Sebastien, Mouri, Oussama, Argy, Nicolas, Camille Roussel, Jaureguiberry, Stephane, Perillaud, Claire, Langui, Dominique, Biligui, Sylvestre, Chartrel, Nathalie, Merens, Audrey, Dondorp, Arjen, Houze, Sandrine, Gay, Frederic, Bonnefoy, Serge, Thellier, Marc, Woodrow, Charlie, and Buffet, Pierre
53. Plasmodium falciparum: An intervening sequence in the GBP 130/96 tR gene
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Bonnefoy, Serge, primary and Mercereau-Puijalon, Odile, additional
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- 1989
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54. Plasmodium falciparum: Molecular analysis of a putative protective antigen, the thermostable 96-kDa protein
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Bonnefoy, Serge, primary, Mattei, Denise, additional, Dubremetz, Jean-François, additional, Guillotte, Micheline, additional, Jouin, Hélène, additional, Ozaki, Luiz S., additional, Sibilli, Lise, additional, and Mercereau-Puijalon, Odile, additional
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- 1988
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55. Measuring the Plasmodium falciparumHRP2 protein in blood from artesunate-treated malaria patients predicts post-artesunate delayed hemolysis
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Ndour, Papa Alioune, Larréché, Sébastien, Mouri, Oussama, Argy, Nicolas, Gay, Frédérick, Roussel, Camille, Jauréguiberry, Stéphane, Perillaud, Claire, Langui, Dominique, Biligui, Sylvestre, Chartrel, Nathalie, Mérens, Audrey, Kendjo, Eric, Ghose, Aniruddha, Hassan, Md. Mahtab Uddin, Hossain, Md. Amir, Kingston, Hugh W. F., Plewes, Katherine, Dondorp, Arjen M., Danis, Martin, Houzé, Sandrine, Bonnefoy, Serge, Thellier, Marc, Woodrow, Charles J., and Buffet, Pierre A.
- Abstract
Previously parasitized erythrocytes in patients with severe malaria retain the parasite protein HRP2, which can be used to predict hemolysis induced by the drug artesunate.
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- 2017
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56. A study of the genomic diversity of Plasmodium falciparum in Senegal 2. Typing by the use of the polymerase chain reaction
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Mercereau-Puijalon, Odile, Fandeur, Thierry, Bonnefoy, Serge, Jacquemot, Catherine, and Sarthou, Jean-Louis
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- 1991
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57. Identification of a heat shock-like antigen in P.falciparum, related to the heat shock protein 90 family.
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Jendoubi, Moncef and Bonnefoy, Serge
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- 1988
58. Immunoglobulin response to Plasmodium falciparum RESA proteins in uncomplicated and severe malaria
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Cyril Badaut, Gratien Sagbo, Serge Bonnefoy, Jacqueline Milet, Florence Migot-Nabias, Léa Guyonnet, Firmine Viwami, Philippe Deloron, Francis Layla, Rémy Durand, Emmanuelle Renard, Institut de Recherche Biomédicale des Armée [Brétigny/Orge] (IRBA), Communautés d’universités et établissements Sorbonne Paris Cité (COMUE Sorbonne Paris Cité), Université Sorbonne Paris Cité (USPC) - Chimie ParisTech - Paris Sciences et Lettres (PSL), Mère et enfant face aux infections tropicales (MERIT - UMR_D 216), Institut de Recherche pour le Développement (IRD) - Université Paris Descartes - Paris 5 (UPD5), Laboratoire de Parasitologie-Mycologie, Assistance publique - Hôpitaux de Paris (AP-HP), Centre d'Etude et de Recherche sur le Paludisme Associé à la Grossesse et l'Enfance (CERPAGE) (CERPAGE), Centre d'Etude et de Recherche sur le Paludisme Associé à la Grossesse et l'Enfance (CERPAGE), Service de Pédiatrie, Centre National Hospitalier et Universitaire Hubert K. Maga, Biologie cellulaire des Trypanosomes, Institut Pasteur [Paris] - Institut National de la Santé et de la Recherche Médicale (INSERM), This work was supported by the French Agence Nationale de la Recherche under grant MIE (ANR-08-MIE-031) and CNRS., ANR-08-MIEN-0031, RESAs, Remodelage physiologique et antigénique de la membrane du globule rouge par Plasmodium falciparum: rôle physio-pathologique de la famille des protéines RESA(2008), Université Sorbonne Paris Cité (USPC)-Chimie ParisTech-Université Paris sciences et lettres (PSL), Mère et enfant en milieu tropical : pathogènes, système de santé et transition épidémiologique (MERIT - UMR_D 216), Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre d’Etude et de Recherche sur le Paludisme Associé à la Grossesse et l’Enfance (CERPAGE), University of Abomey Calavi (UAC), Biologie cellulaire des Trypanosomes - Trypanosome Cell Biology, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), ANR-08-MIEN-0031,RESAs,Remodelage physiologique et antigénique de la membrane du globule rouge par Plasmodium falciparum: rôle physio-pathologique de la famille des protéines RESA(2008), Centre d’Etude et de Recherche sur le Paludisme Associé à la Grossesse et l’Enfance [Cotonou, Bénin] (CERPAGE), Université d’Abomey-Calavi = University of Abomey Calavi (UAC), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), BONNEFOY, Serge, and Maladies Infectieuses et environnement - Remodelage physiologique et antigénique de la membrane du globule rouge par Plasmodium falciparum: rôle physio-pathologique de la famille des protéines RESA - - RESAs2008 - ANR-08-MIEN-0031 - MIE - VALID
- Subjects
Male ,Protozoan Proteins ,Antibodies, Protozoan ,MESH: Cytokines/blood ,Gene mutation ,Ring-infected erythrocyte surface antigen ,Immunoglobulin G ,MESH: Child ,MESH: Recombinant Proteins/immunology ,Benin ,MESH: Plasmodium falciparum/immunology ,Malaria, Falciparum ,Child ,MESH: Immunoglobulin G/immunology ,MESH: Antibodies, Protozoan/blood ,biology ,MESH: Infant ,Recombinant Proteins ,3. Good health ,[SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology ,Infectious Diseases ,Child, Preschool ,Ring-infected erythrocyte surface ,severe malaria ,MESH: Benin/epidemiology ,B cell epitope ,Cytokines ,Female ,Antibody ,Protein family ,Plasmodium falciparum ,MESH: Antibodies, Protozoan/immunology ,MESH: Malaria, Falciparum/epidemiology ,antigen ,MESH: Cross-Sectional Studies ,Antigen ,parasitic diseases ,medicine ,Humans ,MESH: Malaria, Falciparum/immunology ,[SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology ,MESH: Humans ,Research ,MESH: Child, Preschool ,Infant ,MESH: Cytokines/immunology ,medicine.disease ,biology.organism_classification ,MESH: Protozoan Proteins/immunology ,Virology ,MESH: Male ,Cross-Sectional Studies ,Parasitology ,Immunology ,biology.protein ,MESH: Immunoglobulin G/blood ,MESH: Female ,Malaria - Abstract
Background The three members of the ring-infected erythrocyte surface antigen (RESA) proteins family share high sequence homologies, which impair the detection and assignment to one or another protein of some pathogenic processes inherent to Plasmodium falciparum malaria. The present study was intended to determine if the antibody and inflammatory responses of children living in a malaria-endemic area varied depending on the RESA-1, RESA-2 or RESA-3 proteins and the severity of the disease, two groups of severe and uncomplicated malaria cases being considered. Methods Two synthetic peptides representing predicted B cell epitopes were designed per RESA protein, all located outside of the 3′ and 5′ repetition blocks, in order to allow an antibody detection specific of each member of the family. Recombinant rRESA-1B and rRESA-3B proteins were also engineered. Two groups of Beninese children admitted to hospital in 2009 for either uncomplicated or severe malaria were compared for their plasma levels of IgG specifically recognizing each recombinant RESA protein or synthetic peptide, and for their plasma inflammatory cytokine levels (IFN-γ, TNF-α and IL-10), taking into account host and parasite genetic factors. Results The absence of IgG cross-reactivity between rRESA proteins and their protein carrier as well as between each RESA peptide and a non-epitopic RESA control peptide validated the use of the engineered recombinant proteins and peptides for the measurement of plasma IgG. Taking into account age, fever duration and parasitaemia, a multiple logistic regression performed on children clustered according to their antibody responses’ profiles concluded to an increased risk of severe malaria for P2 (representative of RESA-1) responders (P = 0.007). Increased IL-10 plasma levels were found in children harbouring multiclonal P. falciparum infections on the basis of the T1526G resa2 gene polymorphism (P = 0.004). Conclusions This study provided novel tools to dissect the seroreactivity against the three members of the RESA protein family and to describe its relation to protection against malaria. It suggested the measurement of plasma antibodies raised against specific peptides to serve as predictive immunologic markers for disease severity. Lastly, it reinforced previous observations linking the T1526G resa2 gene mutation to severe malaria. Electronic supplementary material The online version of this article (doi:10.1186/s12936-015-0799-8) contains supplementary material, which is available to authorized users.
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- 2015
59. Biallelic Mutations in LRRC56, Encoding a Protein Associated with Intraflagellar Transport, Cause Mucociliary Clearance and Laterality Defects.
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Bonnefoy S, Watson CM, Kernohan KD, Lemos M, Hutchinson S, Poulter JA, Crinnion LA, Berry I, Simmonds J, Vasudevan P, O'Callaghan C, Hirst RA, Rutman A, Huang L, Hartley T, Grynspan D, Moya E, Li C, Carr IM, Bonthron DT, Leroux M, Boycott KM, Bastin P, and Sheridan EG
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- Adult, Alleles, Axoneme genetics, Cell Line, Chlamydomonas genetics, Cilia genetics, Dyneins genetics, Epithelial Cells pathology, Female, HEK293 Cells, Humans, Infant, Male, Phenotype, Trypanosoma brucei brucei genetics, Biological Transport genetics, Flagella genetics, Mucociliary Clearance genetics, Mutation genetics, Proteins genetics
- Abstract
Primary defects in motile cilia result in dysfunction of the apparatus responsible for generating fluid flows. Defects in these mechanisms underlie disorders characterized by poor mucus clearance, resulting in susceptibility to chronic recurrent respiratory infections, often associated with infertility; laterality defects occur in about 50% of such individuals. Here we report biallelic variants in LRRC56 (known as oda8 in Chlamydomonas) identified in three unrelated families. The phenotype comprises laterality defects and chronic pulmonary infections. High-speed video microscopy of cultured epithelial cells from an affected individual showed severely dyskinetic cilia but no obvious ultra-structural abnormalities on routine transmission electron microscopy (TEM). Further investigation revealed that LRRC56 interacts with the intraflagellar transport (IFT) protein IFT88. The link with IFT was interrogated in Trypanosoma brucei. In this protist, LRRC56 is recruited to the cilium during axoneme construction, where it co-localizes with IFT trains and is required for the addition of dynein arms to the distal end of the flagellum. In T. brucei carrying LRRC56-null mutations, or a variant resulting in the p.Leu259Pro substitution corresponding to the p.Leu140Pro variant seen in one of the affected families, we observed abnormal ciliary beat patterns and an absence of outer dynein arms restricted to the distal portion of the axoneme. Together, our findings confirm that deleterious variants in LRRC56 result in a human disease and suggest that this protein has a likely role in dynein transport during cilia assembly that is evolutionarily important for cilia motility., (Copyright © 2018. Published by Elsevier Inc.)
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- 2018
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60. Measuring the Plasmodium falciparum HRP2 protein in blood from artesunate-treated malaria patients predicts post-artesunate delayed hemolysis.
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Ndour PA, Larréché S, Mouri O, Argy N, Gay F, Roussel C, Jauréguiberry S, Perillaud C, Langui D, Biligui S, Chartrel N, Mérens A, Kendjo E, Ghose A, Hassan MMU, Hossain MA, Kingston HWF, Plewes K, Dondorp AM, Danis M, Houzé S, Bonnefoy S, Thellier M, Woodrow CJ, and Buffet PA
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- Adolescent, Adult, Aged, Artemisinins pharmacology, Artesunate, Cytosol metabolism, Demography, Erythrocyte Membrane drug effects, Erythrocyte Membrane metabolism, Erythrocytes drug effects, Erythrocytes parasitology, Erythrocytes ultrastructure, Female, Humans, Malaria parasitology, Male, Middle Aged, Plasmodium falciparum drug effects, Plasmodium falciparum pathogenicity, Quinine pharmacology, Quinine therapeutic use, Young Adult, Antigens, Protozoan blood, Artemisinins therapeutic use, Hemolysis, Malaria blood, Malaria drug therapy, Plasmodium falciparum metabolism, Protozoan Proteins blood
- Abstract
Artesunate, the recommended drug for severe malaria, rapidly clears the malaria parasite from infected patients but frequently induces anemia-called post-artesunate delayed hemolysis (PADH)-for which a simple predictive test is urgently needed. The underlying event in PADH is the expulsion of artesunate-exposed parasites from their host erythrocytes by pitting. We show that the histidine-rich protein 2 (HRP2) of the malaria parasite Plasmodium falciparum persists in the circulation of artesunate-treated malaria patients in Bangladesh and in French travelers who became infected with malaria in Africa. HRP2 persisted in whole blood (not plasma) of artesunate-treated patients with malaria at higher levels compared to quinine-treated patients. Using an optimized membrane permeabilization method, HRP2 was observed by immunofluorescence, Western blotting, and electron microscopy to persist in once-infected red blood cells from artesunate-treated malaria patients. HRP2 was deposited at the membrane of once-infected red blood cells in a pattern similar to that for ring erythrocyte surface antigen (RESA), a parasite invasion marker. On the basis of these observations, we developed a semiquantitative titration method using a widely available HRP2-based rapid diagnostic dipstick test. Positivity on this test using a 1:500 dilution of whole blood from artesunate-treated patients with malaria collected shortly after parasite clearance predicted subsequent PADH with 89% sensitivity and 73% specificity. These results suggest that adapting an existing HRP2-based rapid diagnostic dipstick test may enable prediction of PADH several days before it occurs in artesunate-treated patients with malaria., (Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
- Published
- 2017
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