Accelerated Clearance of Plasmodium-infected Erythrocytes in Sickle Cell Trait and Annexin-A7 Deficiency

被引：124

作者：

Lang, Philipp A. ^{[2
]}

Kasinathan, Ravi S. ^{[2
]}

Brand, Verena B. ^{[2
,9
]}

Duranton, Christophe ^{[2
,10
]}

Lang, Camelia ^{[2
]}

Koka, Saisudha ^{[2
]}

Shumilina, Ekaterina ^{[2
]}

Kempe, Daniela S. ^{[2
]}

Tanneur, Valerie ^{[2
]}

Akel, Ahmad ^{[2
]}

Lang, Karl S. ^{[2
]}

Foeller, Michael ^{[2
]}

Kun, Juergen F. J. ^{[3
]}

Kremsner, Peter G. ^{[3
]}

Wesselborg, Sebastian ^{[4
]}

Laufer, Stefan ^{[5
]}

Clemen, Christoph S. ^{[6
,7
]}

Herr, Claudia ^{[6
,7
]}

Noegel, Angelika A. ^{[6
,7
]}

Wieder, Thomas ^{[11
]}

Gulbins, Erich ^{[8
]}

Lang, Florian ^{[2
]}

Huber, Stephan M. ^{[1
]}

机构：

[1] Univ Tubingen, Dept Radiat Oncol, D-72076 Tubingen, Germany

[2] Univ Tubingen, Dept Physiol, D-72076 Tubingen, Germany

[3] Univ Tubingen, Dept Trop Med, D-72076 Tubingen, Germany

[4] Univ Tubingen, Dept Gastroenterol, D-72076 Tubingen, Germany

[5] Univ Tubingen, Dept Pharm, D-72076 Tubingen, Germany

[6] Univ Cologne, Fac Med, Inst Biochem 1, Ctr Biochem, D-5000 Cologne 41, Germany

[7] Univ Cologne, Ctr Mol Med, D-5000 Cologne 41, Germany

[8] Univ Duisburg Essen, Dept Mol Biol, Essen, Germany

[9] Univ Toronto, Struct Genom Consortium, Toronto, ON M5S 1A1, Canada

[10] Univ Nice, TIANP, CNRS, FRE3093, F-06108 Nice 2, France

[11] Univ Tubingen, Dept Dermatol, D-72076 Tubingen, Germany

来源：

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY | 2009年 / 24卷 / 5-6期

关键词：

Annexin-A7; Ca2+-permeability; Calpain; Phagocytosis; Phospholipid asymmetry; Plasmodium falciparum; Prostaglandin E-2; MEMBRANE PHOSPHOLIPID ORGANIZATION; RED-BLOOD-CELLS; PLASMA-MEMBRANE; APOPTOTIC CELLS; SUICIDAL DEATH; IN-VIVO; MALARIA; FALCIPARUM; PHOSPHATIDYLSERINE; ERYPTOSIS;

D O I：

10.1159/000257529

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The course of malaria does not only depend on the virulence of the parasite Plasmodium but also on properties of host erythrocytes. Here, we show that infection of erythrocytes from human sickle cell trait (HbA/S) carriers with ring stages of P. falciparum led to significantly enhanced PGE(2) formation, Ca2+ permeability, annexin-A7 degradation, phosphatidylserine (PS) exposure at the cell surface, and clearance by macrophages. P. berghei-infected erythrocytes from annexin-A7-deficient (annexin-A7(-/-)) mice were more rapidly cleared than infected wildtype cells. Accordingly, P. berghei-infected annexin-A7(-/-) mice developed less parasitemia than wildtype mice. The cyclooxygenase inhibitor aspirin decreased erythrocyte PS exposure in infected annexin-A7(-/-) mice and abolished the differences of parasitemia and survival between the genotypes. Conversely, the PGE(2)-agonist sulprostone decreased parasitemia and increased survival of wild type mice. In conclusion, PS exposure on erythrocytes results in accelerated clearance of Plasmodium ring stage-infected HbA/S or annexin-A7(-/-) erythrocytes and thus confers partial protection against malaria in vivo. Copyright (C) 2009 S. Karger AG, Basel

引用

页码：415 / 428

页数：14

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