scholarly journals Characterization of the complement sensitivity of calcium loaded human erythrocytes

Blood ◽  
1991 ◽  
Vol 78 (11) ◽  
pp. 3056-3065 ◽  
Author(s):  
ST Test ◽  
P Butikofer ◽  
MC Yee ◽  
FA Kuypers ◽  
B Lubin

Abstract A deficiency of membrane proteins having a glycosylphosphatidylinositol (GPI) anchor is characteristic of the erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH) and is currently believed to be the basis for the enhanced susceptibility to lysis by activated complement observed in these cells. Our recent observation that GPI-anchored proteins are preferentially lost into membrane vesicles shed from normal erythrocytes after calcium loading led us to examine the hypothesis that the remnant erythrocytes might also have increased sensitivity to complement-mediated hemolysis. Indeed, red blood cells treated in such a manner became more sensitive to lysis by antibody and complement or to lysis initiated by activated cobra venom factor complexes (CoFBb). As a consequence of membrane vesiculation, the erythrocytes lost up to approximately 50% of their immunoreactive decay- accelerating factor and 25% to 30% of their immunoreactive membrane inhibitor of reactive lysis (MIRL). Closer examination of the defect responsible for the marked increase in sensitivity to CoFBb-initiated hemolysis seen in calcium-loaded erythrocytes showed that a complex combination of factors produced the defect. These included a decrease in both functional and immunoreactive MIRL and depletion of intracellular potassium and adenosine triphosphate (ATP). These results suggest the possibility that loss of DAF and MIRL via membrane vesiculation, as well as decreases in intracellular potassium and/or ATP, might contribute to the phenotype of PNH erythrocytes. Further, normal or pathologic red blood cells might develop a PNH-like defect after membrane vesiculation if sufficient decreases in potassium and ATP also occurred.

Blood ◽  
1991 ◽  
Vol 78 (11) ◽  
pp. 3056-3065 ◽  
Author(s):  
ST Test ◽  
P Butikofer ◽  
MC Yee ◽  
FA Kuypers ◽  
B Lubin

A deficiency of membrane proteins having a glycosylphosphatidylinositol (GPI) anchor is characteristic of the erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH) and is currently believed to be the basis for the enhanced susceptibility to lysis by activated complement observed in these cells. Our recent observation that GPI-anchored proteins are preferentially lost into membrane vesicles shed from normal erythrocytes after calcium loading led us to examine the hypothesis that the remnant erythrocytes might also have increased sensitivity to complement-mediated hemolysis. Indeed, red blood cells treated in such a manner became more sensitive to lysis by antibody and complement or to lysis initiated by activated cobra venom factor complexes (CoFBb). As a consequence of membrane vesiculation, the erythrocytes lost up to approximately 50% of their immunoreactive decay- accelerating factor and 25% to 30% of their immunoreactive membrane inhibitor of reactive lysis (MIRL). Closer examination of the defect responsible for the marked increase in sensitivity to CoFBb-initiated hemolysis seen in calcium-loaded erythrocytes showed that a complex combination of factors produced the defect. These included a decrease in both functional and immunoreactive MIRL and depletion of intracellular potassium and adenosine triphosphate (ATP). These results suggest the possibility that loss of DAF and MIRL via membrane vesiculation, as well as decreases in intracellular potassium and/or ATP, might contribute to the phenotype of PNH erythrocytes. Further, normal or pathologic red blood cells might develop a PNH-like defect after membrane vesiculation if sufficient decreases in potassium and ATP also occurred.


Lab on a Chip ◽  
2021 ◽  
Author(s):  
YUHAO QIANG ◽  
Jia Liu ◽  
Ming Dao ◽  
E Du

Red blood cells (RBCs) are subjected to recurrent changes in shear stress and oxygen tension during blood circulation. The cyclic shear stress has been identified as an important factor that...


2016 ◽  
Vol 100 ◽  
pp. S193
Author(s):  
Joo-Yeun Oh ◽  
Xin Xu ◽  
Kristopher Genschmer ◽  
Ming Zhong ◽  
Jindong Li ◽  
...  
Keyword(s):  

2021 ◽  
Vol 15 (02) ◽  
pp. 270-279
Author(s):  
Aline Griebler ◽  
Fernanda Weyand Banhuk ◽  
Izabela Virginia Staffen ◽  
Aline Antunes Maciel Bortoluzzi ◽  
Thaís Soprani Ayala ◽  
...  

Introduction: Trypanosoma cruzi is the agent of Chagas’ disease and affects approximately 6-8 million people worldwide. The search for new anti-T. cruzi drugs are relevant because only two drugs exist actually. The objective of this study was to investigate the effect of the extracts from the seeds of Lonchocarpus cultratus on T. cruzi, its cytotoxicity as well as to elucidate its chemical profile. Methodology: The characterization of the extracts was done using 1H-RMN. T. cruzi forms were treated with increasing concentrations of the extracts and after, the percentage of inhibition and IC50 or LC50 were calculated. Murine peritoneal macrophages were treated with different concentrations of the extracts to evaluate the cellular viability. The hemotoxicity was accessed by verifying the levels of hemolysis caused by the extracts on human red blood cells. Results: Chalcones isocordoin and lonchocarpin were detected in the dichloromethane extract, and chalcone lonchocarpin was detected in the hexane extract. The dichloromethane extract showed higher activity against all the forms of T. cruzi compared to the other two extracts, but the hexane showed the best selectivity index. The cytotoxicity observed in murine macrophages was confirmed in human erythrocytes, with dichloromethane extract having the highest toxicity. The methanolic extract showed the lowest anti-T. cruzi activity but was nontoxic to peritoneal murine macrophages and red blood cells. Conclusions: L. cultratus extracts have the potential to be explored for the development of new anti-trypanosomal drugs. This study was the first to demonstrate the action of extracts from the genus Lonchocarpus on infecting forms of T. cruzi.


Lab on a Chip ◽  
2020 ◽  
Vol 20 (2) ◽  
pp. 226-235 ◽  
Author(s):  
Emel Islamzada ◽  
Kerryn Matthews ◽  
Quan Guo ◽  
Aline T. Santoso ◽  
Simon P. Duffy ◽  
...  

Cell sorting using microfluidic ratchets enables sensitive and consistent characterization of donor red blood cell deformability. Using this capability, we show the degradation of red blood cell deformability during cold storage is donor-dependent.


Blood ◽  
2004 ◽  
Vol 104 (9) ◽  
pp. 2961-2966 ◽  
Author(s):  
Alfred Cortés ◽  
Ariadna Benet ◽  
Brian M. Cooke ◽  
John W. Barnwell ◽  
John C. Reeder

Abstract Plasmodium falciparum, the causative agent of the most lethal form of human malaria, uses multiple ligand-receptor interactions to invade host red blood cells (RBCs). We studied the invasion of P falciparum into abnormal RBCs from humans carrying the Southeast Asian ovalocytosis (SAO) trait. One particular parasite line, 3D7-A, invaded these cells efficiently, whereas all other lines studied invaded SAO RBCs to only about 20% of the extent of normal (non-SAO) cells. This result is consistent with the clinical observation that SAO individuals can experience high-density P falciparum infections and provides an explanation for previous discrepant results on invasion of SAO RBCs. Characterization of the invasion phenotype of 3D7-A revealed that efficient invasion of SAO RBCs was paralleled by relatively efficient invasion of normal RBCs treated with either neuraminidase, trypsin, or chymotrypsin and a novel capacity to invade normal RBCs treated sequentially with both neuraminidase and trypsin. Our results suggest that only parasites able to use some particular invasion pathways can invade SAO RBCs efficiently in culture. A similar situation might occur in the field.


Sign in / Sign up

Export Citation Format

Share Document