Absence of erythrocyte sequestration and lack of multicopy gene family expression in Plasmodium falciparum from a splenectomized malaria patient.
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Absence of erythrocyte sequestration and lack of multicopy gene family expression in Plasmodium falciparum from a splenectomized malaria patient. / Bachmann, Anna; Esser, Claudia; Petter, Michaela; Predehl, Sabine; Von Kalckreuth, Vera; Schmiedel, Stefan; Bruchhaus, Iris; Tannich, Egbert.
In: PLOS ONE, Vol. 4, No. 10, 10, 2009, p. 7459.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Absence of erythrocyte sequestration and lack of multicopy gene family expression in Plasmodium falciparum from a splenectomized malaria patient.
AU - Bachmann, Anna
AU - Esser, Claudia
AU - Petter, Michaela
AU - Predehl, Sabine
AU - Von Kalckreuth, Vera
AU - Schmiedel, Stefan
AU - Bruchhaus, Iris
AU - Tannich, Egbert
PY - 2009
Y1 - 2009
N2 - BACKGROUND: To avoid spleen-dependent killing mechanisms parasite-infected erythrocytes (IE) of Plasmodium falciparum malaria patients have the capacity to bind to endothelial receptors. This binding also known as sequestration, is mediated by parasite proteins, which are targeted to the erythrocyte surface. Candidate proteins are those encoded by P. falciparum multicopy gene families, such as var, rif, stevor or PfMC-2TM. However, a direct in vivo proof of IE sequestration and expression of multicopy gene families is still lacking. Here, we report on the analysis of IE from a black African immigrant, who received the diagnosis of a malignant lymphoproliferative disorder and subsequently underwent splenectomy. Three weeks after surgery, the patient experienced clinical falciparum malaria with high parasitemia and circulating developmental parasite stages usually sequestered to the vascular endothelium such as late trophozoites, schizonts or immature gametocytes. METHODOLOGY/PRINCIPAL FINDINGS: Initially, when isolated from the patient, the infected erythrocytes were incapable to bind to various endothelial receptors in vitro. Moreover, the parasites failed to express the multicopy gene families var, A-type rif and stevor but expression of B-type rif and PfMC-2TM genes were detected. In the course of in vitro cultivation, the parasites started to express all investigated multicopy gene families and concomitantly developed the ability to adhere to endothelial receptors such as CD36 and ICAM-1, respectively. CONCLUSION/SIGNIFICANCE: This case strongly supports the hypothesis that parasite surface proteins such as PfEMP1, A-type RIFIN or STEVOR are involved in interactions of infected erythrocytes with endothelial receptors mediating sequestration of mature asexual and immature sexual stages of P. falciparum. In contrast, multicopy gene families coding for B-type RIFIN and PfMC-2TM proteins may not be involved in sequestration, as these genes were transcribed in infected but not sequestered erythrocytes.
AB - BACKGROUND: To avoid spleen-dependent killing mechanisms parasite-infected erythrocytes (IE) of Plasmodium falciparum malaria patients have the capacity to bind to endothelial receptors. This binding also known as sequestration, is mediated by parasite proteins, which are targeted to the erythrocyte surface. Candidate proteins are those encoded by P. falciparum multicopy gene families, such as var, rif, stevor or PfMC-2TM. However, a direct in vivo proof of IE sequestration and expression of multicopy gene families is still lacking. Here, we report on the analysis of IE from a black African immigrant, who received the diagnosis of a malignant lymphoproliferative disorder and subsequently underwent splenectomy. Three weeks after surgery, the patient experienced clinical falciparum malaria with high parasitemia and circulating developmental parasite stages usually sequestered to the vascular endothelium such as late trophozoites, schizonts or immature gametocytes. METHODOLOGY/PRINCIPAL FINDINGS: Initially, when isolated from the patient, the infected erythrocytes were incapable to bind to various endothelial receptors in vitro. Moreover, the parasites failed to express the multicopy gene families var, A-type rif and stevor but expression of B-type rif and PfMC-2TM genes were detected. In the course of in vitro cultivation, the parasites started to express all investigated multicopy gene families and concomitantly developed the ability to adhere to endothelial receptors such as CD36 and ICAM-1, respectively. CONCLUSION/SIGNIFICANCE: This case strongly supports the hypothesis that parasite surface proteins such as PfEMP1, A-type RIFIN or STEVOR are involved in interactions of infected erythrocytes with endothelial receptors mediating sequestration of mature asexual and immature sexual stages of P. falciparum. In contrast, multicopy gene families coding for B-type RIFIN and PfMC-2TM proteins may not be involved in sequestration, as these genes were transcribed in infected but not sequestered erythrocytes.
KW - Animals
KW - Humans
KW - Female
KW - Middle Aged
KW - DNA Primers chemistry
KW - Endothelium, Vascular cytology
KW - Erythrocyte Membrane metabolism
KW - Erythrocytes cytology
KW - Gene Expression Regulation
KW - Lymphoproliferative Disorders complications
KW - Malaria blood
KW - Merozoite Surface Protein 1 metabolism
KW - Multigene Family
KW - Plasmodium falciparum metabolism
KW - Splenectomy
KW - Animals
KW - Humans
KW - Female
KW - Middle Aged
KW - DNA Primers chemistry
KW - Endothelium, Vascular cytology
KW - Erythrocyte Membrane metabolism
KW - Erythrocytes cytology
KW - Gene Expression Regulation
KW - Lymphoproliferative Disorders complications
KW - Malaria blood
KW - Merozoite Surface Protein 1 metabolism
KW - Multigene Family
KW - Plasmodium falciparum metabolism
KW - Splenectomy
U2 - 10.1371/journal.pone.0007459
DO - 10.1371/journal.pone.0007459
M3 - SCORING: Zeitschriftenaufsatz
VL - 4
SP - 7459
JO - PLOS ONE
JF - PLOS ONE
SN - 1932-6203
IS - 10
M1 - 10
ER -
