title: In vitro RBC exposure to Plasmodium falciparum has no effect on RBC antigen expression.
abstract: Severe malarial anaemia is a leading cause of death in African children younger than 3 years of age who are infected with Plasmodium falciparum. The pathogenesis of this anaemia is not understood. The purpose of this study was to determine if P. falciparum induces changes in RBC membranes that contribute to the immune destruction of RBCs. RBCs were collected from healthy subjects and tested using standard haemagglutination assays for 45 antigens representing 21 blood group systems/collections before and after exposure to P. falciparum, strain FVO. Lectins were used to determine whether crypt or neoantigens were expressed on the RBC membrane. Polybrene was used to detect changes in sialic acid. RBCs were cultured in vitro with and without the parasite, and blinded serologic studies were completed. CD35 (complement receptor 1), CD55 (decay-accelerating factor), CD59 (membrane inhibitor of reactive lysis) and CD47 (integrin-associated protein) flow cytometric assays were compared for infected and uninfected RBCs. The percentage of parasitaemia was determined using Giemsa-stained thin blood films. Two (Ch, Lub) of the 45 antigens had differing strengths of agglutination between infected and uninfected RBCs, but these differences were resolved with a second source of antisera. Forty-three antigens showed no significant differences in the strength of agglutination between the infected and uninfected RBCs. Lectin and polybrene testing showed no differences. CD35, CD55, CD59 and CD47 levels showed no significant differences. P. falciparum does not appear to alter the expression of classified immunogenic antigens on the RBC membrane in this in vitro system. The pathogenesis of the haemolytic episode that occurs in these children remains unclear.
authors.affiliation: Department of Transfusion Medicine, Warren G. Magnuson Clinical Center, National Institute of Allergy and Infectious Diseases/NIH, Building 10, Room 1C711, 120 Center Drive, Bethesda, MD 20892, USA.
authors.forename: D R
authors.initials: DR
authors.lastname: Chambers
authors.forename: J
authors.initials: J
authors.lastname: Procter
authors.forename: O
authors.initials: O
authors.lastname: Muratova
authors.forename: K
authors.initials: K
authors.lastname: Byrne
authors.forename: D
authors.initials: D
authors.lastname: Keister
authors.forename: D
authors.initials: D
authors.lastname: Shanks
authors.forename: A
authors.initials: A
authors.lastname: Magill
authors.forename: D
authors.initials: D
authors.lastname: Stroncek
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D001742:Blackwater Fever / Q000209:etiology; D001789:Blood Group Antigens / Q000276:immunology; D051928:CD47 Antigen; D018958:CD55 Antigens / Q000032:analysis; D018957:CD59 Antigens / Q000032:analysis; D002352:Carrier Proteins / Q000032:analysis; D018929:Cell Culture Techniques; D004912:Erythrocytes / Q000276:immunology / Q000469:parasitology*; D005434:Flow Cytometry; D006386:Hemagglutination Tests; D006801:Humans; D007519:Isoantigens / Q000032:analysis*; D010963:Plasmodium falciparum / Q000276:immunology*; D017463:Receptors, Complement 3b / Q000032:analysis
chemical_list: D015703:Antigens, CD; D001789:Blood Group Antigens; D051928:CD47 Antigen; C497894:CD47 protein, human; D018958:CD55 Antigens; D018957:CD59 Antigens; D002352:Carrier Proteins; D007519:Isoantigens; D017463:Receptors, Complement 3b