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-
1
Waitumbi JN, Opollo MO, Muga RO, Misore AO, Stoute JA, 2000. Red cell surface changes and erythrophagocytosis in children with severe Plasmodium falciparum anemia. Blood 95 :1481–1486.
-
2
Takeda J, Miyata T, Kawagoe K, Iida Y, Endo Y, Fujita T, Takahashi M, Kitani T, Kinoshita T, 1993. Deficiency of the GPI anchor caused by a somatic mutation of the PIG-A gene in paroxysmal nocturnal hemoglobinuria. Cell 73 :703–711.
-
3
Samuel BU, Mohandas N, Harrison T, McManus H, Rosse W, Reid M, Haldar K, 2001. The role of cholesterol and glycosylphosphatidylinositol-anchored proteins of erythrocyte rafts in regulating raft protein content and malarial infection. J Biol Chem 276 :29319–29329.
-
4
Wiesner J, Jomaa H, Wilhelm M, Tony HP, Kremsner PG, Horrocks P, Lanzer M, 1997. Host cell factor CD59 restricts complement lysis of Plasmodium falciparum-infected erythrocytes. Eur J Immunol 27 :2708–2713.
-
5
Chitnis CE, 2001. Molecular insights into receptors used by malaria parasites for erythrocyte invasion. Curr Opin Hematol 8 :85–91.
-
6
Chitnis CE, Blackman MJ, 2000. Host cell invasion by malaria parasites. Parasitol Today 16 :411–415.
-
7
Soubes SC, Reid ME, Kaneko O, Miller LH, 1999. Search for the sialic acid-independent receptor on red blood cells for invasion by Plasmodium falciparum. Vox Sang 76 :107–114.
-
8
Pattanapanyasat K, Yongvanitchit K, Heppner DG, Tongtawe P, Kyle DE, Webster HK, 1996. Culture of malaria parasites in two different red blood cell populations using biotin and flow cytometry. Cytometry 25 :287–294.
-
9
Pattanapanyasat K, Yongvanitchit K, Tongtawe P, Tachavanich K, Wanachiwanawin W, Fucharoen S, Walsh DS, 1999. Impairment of Plasmodium falciparum growth in thalassemic red blood cells: further evidence by using biotin labeling and flow cytometry. Blood 93 :3116–3119.
-
10
Trager W, Jensen JB, 1976. Human malaria parasites in continuous culture. Science 193 :673–675.
-
11
Lambros C, Vanderberg JP, 1979. Synchronization of Plasmodium falciparum erythrocytic stages in culture. J Parasitol 65 :418–420.
-
12
Rosse WF, Nishimura J, 2003. Clinical manifestations of paroxysmal nocturnal hemoglobinuria: present state and future problems. Int J Hematol 77 :113–120.
-
13
Rosse WF, 2001. New insights into paroxysmal nocturnal hemoglobinuria. Curr Opin Hematol 8 :61–67.
-
14
Hall SE, Rosse WF, 1996. The use of monoclonal antibodies and flow cytometry in the diagnosis of paroxysmal nocturnal hemoglobinuria. Blood 87 :5332–5340.
-
15
Mitchell GH, Hadley TJ, McGinniss MH, Klotz FW, Miller LH, 1986. Invasion of erythrocytes by Plasmodium falciparum malaria parasites: evidence for receptor heterogeneity and two receptors. Blood 67 :1519–1521.
-
16
Doolan DL, Hedstrom RC, Gardner MJ, Sedegah M, Wang H, Gramzinski RA, Margalith M, Hobart P, Hoffman SL, 1998. DNA vaccination as an approach to malaria control: current status and strategies. Curr Top Microbiol Immunol 226 :37–56.
-
17
Pasvol G, Wilson RJ, 1982. The interaction of malaria parasites with red blood cells. Br Med Bull 38 :133–140.
-
18
Rabesandratana H, Toutant JP, Reggio H, Vidal M, 1998. Decay-accelerating factor (CD55) and membrane inhibitor of reactive lysis (CD59) are released within exosomes during in vitro maturation of reticulocytes. Blood 91 :2573–2580.
-
19
Navenot JM, Muller JY, Blanchard D, 1998. Investigation of the survival of paroxysmal nocturnal hemoglobinuria red cells through the immunophenotyping of reticulocytes. Transfusion 38 :337–342.
-
20
Nishimura J, Smith CA, Phillips KL, Ware RE, Rosse WF, 1998. Paroxysmal nocturnal hemoglobinuria: molecular pathogenesis and molecular therapeutic approaches. Hematopathol Mol Hematol 11 :119–146.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 13 | 13 | 4 |
| Full Text Views | 230 | 82 | 2 |
| PDF Downloads | 45 | 24 | 3 |
ROBUST IN VITRO REPLICATION OF PLASMODIUM FALCIPARUM IN GLYCOSYL-PHOSPHATIDYLINOSITOL–ANCHORED MEMBRANE GLYCOPROTEIN–DEFICIENT RED BLOOD CELLS
KOVIT PATTANAPANYASAT
KOVIT PATTANAPANYASAT
Center of Excellence for Flow Cytometry, Office for Research and Development, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; Becton Dickinson Biosciences, San Jose, California
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DOUGLAS S. WALSH
DOUGLAS S. WALSH
Center of Excellence for Flow Cytometry, Office for Research and Development, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; Becton Dickinson Biosciences, San Jose, California
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KOSOL YONGVANITCHIT
KOSOL YONGVANITCHIT
Center of Excellence for Flow Cytometry, Office for Research and Development, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; Becton Dickinson Biosciences, San Jose, California
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NATAWAN PIYAWATTHANASAKUL
NATAWAN PIYAWATTHANASAKUL
Center of Excellence for Flow Cytometry, Office for Research and Development, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; Becton Dickinson Biosciences, San Jose, California
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WANCHAI WANACHIWANAWIN
WANCHAI WANACHIWANAWIN
Center of Excellence for Flow Cytometry, Office for Research and Development, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; Becton Dickinson Biosciences, San Jose, California
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H. KYLE WEBSTER
H. KYLE WEBSTER
Center of Excellence for Flow Cytometry, Office for Research and Development, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; Becton Dickinson Biosciences, San Jose, California
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Red blood cells (RBCs) infected with Plasmodium falciparum are protected from complement-mediated lysis by surface membrane glycosylphosphatidylinositol (GPI)-anchored proteins, which include decay accelerating factor (DAF or CD55) and CD59. To determine if P. falciparum avoids or replicates less efficiently in GPI protein-deficient cells at a higher risk for complement-mediated lysis, we compared P. falciparum infectivity among control RBCs with those from subjects with paroxysmal nocturnal hemoglobinuria (PNH), a condition in which RBCs express variable levels of DAF (negative and positive) and CD59 (negative [−], intermediate [I], and high [H]). Co-cultures of 19 matched samples of control and PNH RBCs were infected with P. falciparum to directly compare parasitic invasion. Each PNH RBC sample was then assessed for P. falciparum infectivity across the spectrum of GPI protein deficiency. Identification methods included biotin-streptavidin for RBC populations, fluorescein isothiocyanate-labeled antibodies to DAF and CD59, hydroethidine for parasite DNA, and flow cytometry. The mean ± SD parasitemias in co-cultured PNH and control RBCs were 24.7 ± 6.9% versus 21.0 ± 5.9% (P 30.12). For individual PNH samples, parasitemias were significantly higher in DAF (−) cells versus DAF (+) cells (25.0 ± 8.9% versus 19.1 ± 8.7%; P < 0.001) and in CD59 (−) cells versus I/H cells (22.5 ± 6.4% versus 17.6 ± 4.2%; P < 0.0003). Across the CD59 spectrum, mean parasitemias were highest in CD59 (−) cells (24.5 ± 6.4%), followed by CD59-H cells (19.5 ± 5.4%), and CD59-I cells (16.4 ± 4.8%). Expression of DAF in 12 (63%) of 19 infected PNH samples was reduced. Thus, P. falciparum does not selectively avoid RBCs with fewer GPI proteins and parasite replication in PNH cells is at least as robust as in normal RBCs.
Author Notes
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
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-
1
Waitumbi JN, Opollo MO, Muga RO, Misore AO, Stoute JA, 2000. Red cell surface changes and erythrophagocytosis in children with severe Plasmodium falciparum anemia. Blood 95 :1481–1486.
-
2
Takeda J, Miyata T, Kawagoe K, Iida Y, Endo Y, Fujita T, Takahashi M, Kitani T, Kinoshita T, 1993. Deficiency of the GPI anchor caused by a somatic mutation of the PIG-A gene in paroxysmal nocturnal hemoglobinuria. Cell 73 :703–711.
-
3
Samuel BU, Mohandas N, Harrison T, McManus H, Rosse W, Reid M, Haldar K, 2001. The role of cholesterol and glycosylphosphatidylinositol-anchored proteins of erythrocyte rafts in regulating raft protein content and malarial infection. J Biol Chem 276 :29319–29329.
-
4
Wiesner J, Jomaa H, Wilhelm M, Tony HP, Kremsner PG, Horrocks P, Lanzer M, 1997. Host cell factor CD59 restricts complement lysis of Plasmodium falciparum-infected erythrocytes. Eur J Immunol 27 :2708–2713.
-
5
Chitnis CE, 2001. Molecular insights into receptors used by malaria parasites for erythrocyte invasion. Curr Opin Hematol 8 :85–91.
-
6
Chitnis CE, Blackman MJ, 2000. Host cell invasion by malaria parasites. Parasitol Today 16 :411–415.
-
7
Soubes SC, Reid ME, Kaneko O, Miller LH, 1999. Search for the sialic acid-independent receptor on red blood cells for invasion by Plasmodium falciparum. Vox Sang 76 :107–114.
-
8
Pattanapanyasat K, Yongvanitchit K, Heppner DG, Tongtawe P, Kyle DE, Webster HK, 1996. Culture of malaria parasites in two different red blood cell populations using biotin and flow cytometry. Cytometry 25 :287–294.
-
9
Pattanapanyasat K, Yongvanitchit K, Tongtawe P, Tachavanich K, Wanachiwanawin W, Fucharoen S, Walsh DS, 1999. Impairment of Plasmodium falciparum growth in thalassemic red blood cells: further evidence by using biotin labeling and flow cytometry. Blood 93 :3116–3119.
-
10
Trager W, Jensen JB, 1976. Human malaria parasites in continuous culture. Science 193 :673–675.
-
11
Lambros C, Vanderberg JP, 1979. Synchronization of Plasmodium falciparum erythrocytic stages in culture. J Parasitol 65 :418–420.
-
12
Rosse WF, Nishimura J, 2003. Clinical manifestations of paroxysmal nocturnal hemoglobinuria: present state and future problems. Int J Hematol 77 :113–120.
-
13
Rosse WF, 2001. New insights into paroxysmal nocturnal hemoglobinuria. Curr Opin Hematol 8 :61–67.
-
14
Hall SE, Rosse WF, 1996. The use of monoclonal antibodies and flow cytometry in the diagnosis of paroxysmal nocturnal hemoglobinuria. Blood 87 :5332–5340.
-
15
Mitchell GH, Hadley TJ, McGinniss MH, Klotz FW, Miller LH, 1986. Invasion of erythrocytes by Plasmodium falciparum malaria parasites: evidence for receptor heterogeneity and two receptors. Blood 67 :1519–1521.
-
16
Doolan DL, Hedstrom RC, Gardner MJ, Sedegah M, Wang H, Gramzinski RA, Margalith M, Hobart P, Hoffman SL, 1998. DNA vaccination as an approach to malaria control: current status and strategies. Curr Top Microbiol Immunol 226 :37–56.
-
17
Pasvol G, Wilson RJ, 1982. The interaction of malaria parasites with red blood cells. Br Med Bull 38 :133–140.
-
18
Rabesandratana H, Toutant JP, Reggio H, Vidal M, 1998. Decay-accelerating factor (CD55) and membrane inhibitor of reactive lysis (CD59) are released within exosomes during in vitro maturation of reticulocytes. Blood 91 :2573–2580.
-
19
Navenot JM, Muller JY, Blanchard D, 1998. Investigation of the survival of paroxysmal nocturnal hemoglobinuria red cells through the immunophenotyping of reticulocytes. Transfusion 38 :337–342.
-
20
Nishimura J, Smith CA, Phillips KL, Ware RE, Rosse WF, 1998. Paroxysmal nocturnal hemoglobinuria: molecular pathogenesis and molecular therapeutic approaches. Hematopathol Mol Hematol 11 :119–146.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 13 | 13 | 4 |
| Full Text Views | 230 | 82 | 2 |
| PDF Downloads | 45 | 24 | 3 |