Plasmodium falciparum glycosylphosphatidylinositol toxin interacts with the membrane of non-parasitized red blood cells: a putative mechanism contributing to malaria anemia.

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Plasmodium falciparum glycosylphosphatidylinositol toxin interacts with the membrane of non-parasitized red blood cells: a putative mechanism contributing to malaria anemia. / Brattig, Norbert W; Kowalsky, Katharina; Liu, Xinyu; Burchard, Gerd-Dieter; Kamena, Faustin; Seeberger, Peter H.

in: MICROBES INFECT, Jahrgang 10, Nr. 8, 8, 2008, S. 885-891.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{1b73f41bd9e4485baae5eec40d89e8bc,
title = "Plasmodium falciparum glycosylphosphatidylinositol toxin interacts with the membrane of non-parasitized red blood cells: a putative mechanism contributing to malaria anemia.",
abstract = "Following exposure to synthetic Plasmodium falciparum glycosylphosphatidylinositol (P.f.-GPI), red blood cells (RBCs) reacted with antibodies in the serum of a patient with severe acute P. falciparum malaria. Carbohydrate microarray analysis of the patient's serum confirmed the presence of both, IgM and IgG antibodies against P.f.-GPI. The antibodies failed to bind to RBCs when P.f.-GPI lacking the lipid portion was applied. Addition of the detergent Triton X-100 during preincubation with P.f.-GPI resulted in increased recognition. Recognition of P.f.-GPI was dependent on the concentrations of synthetic P.f.-GPI, the serum and the numbers of RBCs. IgM antibodies dominated P.f.-GPI-sensitized RBCs recognition. Recognition by IgM antibodies proved highest during the 1st week of acute malaria and decreased during the following 2 weeks as assessed by flow cytometry and carbohydrate microarray analysis. These results strongly support the notion that released P.f.-GPI can insert into non-parasitized RBC membranes and results in recognition by circulating anti-GPI antibodies and possibly subsequent elimination. This process may contribute to malaria-associated anemia.",
author = "Brattig, {Norbert W} and Katharina Kowalsky and Xinyu Liu and Gerd-Dieter Burchard and Faustin Kamena and Seeberger, {Peter H}",
year = "2008",
language = "Deutsch",
volume = "10",
pages = "885--891",
journal = "MICROBES INFECT",
issn = "1286-4579",
publisher = "Elsevier Masson SAS",
number = "8",

}

RIS

TY - JOUR

T1 - Plasmodium falciparum glycosylphosphatidylinositol toxin interacts with the membrane of non-parasitized red blood cells: a putative mechanism contributing to malaria anemia.

AU - Brattig, Norbert W

AU - Kowalsky, Katharina

AU - Liu, Xinyu

AU - Burchard, Gerd-Dieter

AU - Kamena, Faustin

AU - Seeberger, Peter H

PY - 2008

Y1 - 2008

N2 - Following exposure to synthetic Plasmodium falciparum glycosylphosphatidylinositol (P.f.-GPI), red blood cells (RBCs) reacted with antibodies in the serum of a patient with severe acute P. falciparum malaria. Carbohydrate microarray analysis of the patient's serum confirmed the presence of both, IgM and IgG antibodies against P.f.-GPI. The antibodies failed to bind to RBCs when P.f.-GPI lacking the lipid portion was applied. Addition of the detergent Triton X-100 during preincubation with P.f.-GPI resulted in increased recognition. Recognition of P.f.-GPI was dependent on the concentrations of synthetic P.f.-GPI, the serum and the numbers of RBCs. IgM antibodies dominated P.f.-GPI-sensitized RBCs recognition. Recognition by IgM antibodies proved highest during the 1st week of acute malaria and decreased during the following 2 weeks as assessed by flow cytometry and carbohydrate microarray analysis. These results strongly support the notion that released P.f.-GPI can insert into non-parasitized RBC membranes and results in recognition by circulating anti-GPI antibodies and possibly subsequent elimination. This process may contribute to malaria-associated anemia.

AB - Following exposure to synthetic Plasmodium falciparum glycosylphosphatidylinositol (P.f.-GPI), red blood cells (RBCs) reacted with antibodies in the serum of a patient with severe acute P. falciparum malaria. Carbohydrate microarray analysis of the patient's serum confirmed the presence of both, IgM and IgG antibodies against P.f.-GPI. The antibodies failed to bind to RBCs when P.f.-GPI lacking the lipid portion was applied. Addition of the detergent Triton X-100 during preincubation with P.f.-GPI resulted in increased recognition. Recognition of P.f.-GPI was dependent on the concentrations of synthetic P.f.-GPI, the serum and the numbers of RBCs. IgM antibodies dominated P.f.-GPI-sensitized RBCs recognition. Recognition by IgM antibodies proved highest during the 1st week of acute malaria and decreased during the following 2 weeks as assessed by flow cytometry and carbohydrate microarray analysis. These results strongly support the notion that released P.f.-GPI can insert into non-parasitized RBC membranes and results in recognition by circulating anti-GPI antibodies and possibly subsequent elimination. This process may contribute to malaria-associated anemia.

M3 - SCORING: Zeitschriftenaufsatz

VL - 10

SP - 885

EP - 891

JO - MICROBES INFECT

JF - MICROBES INFECT

SN - 1286-4579

IS - 8

M1 - 8

ER -