Characterization of events preceding the release of malaria parasite from the host red blood cell

2005 ◽  
Vol 35 (2) ◽  
pp. 201-211 ◽  
Author(s):  
Shivani Soni ◽  
Shikha Dhawan ◽  
Kenneth M. Rosen ◽  
Mark Chafel ◽  
Athar H. Chishti ◽  
...  
2020 ◽  
Vol 118 (3) ◽  
pp. 574a
Author(s):  
Matthias Garten ◽  
Josh Beck ◽  
Robyn Roth ◽  
John E. Heuser ◽  
Tatyana Tenkova-Heuser ◽  
...  

2012 ◽  
Author(s):  
Eno Hysi ◽  
Ratan K. Saha ◽  
Min Rui ◽  
Michael C. Kolios

Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1270-1276 ◽  
Author(s):  
TN Estep ◽  
RA Pedersen ◽  
TJ Miller ◽  
KR Stupar

Abstract Di-(2-ethylhexyl) phthalate (DEHP) accumulates in blood brought into contact with materials utilizing this compound as a plasticizer. To determine whether this phthalate diester affects red blood cell integrity, we have compared cell morphology, plasma hemoglobin accumulation, micro-vesicle production, and the concentration of intracellular metabolites and electrolytes of erythrocytes from blood stored at 4 degrees C with and without DEHP. When sufficient emulsified DEHP was mixed with blood to give a final concentration of 300 micrograms/mL, plasma hemoglobin accumulation was reduced by an average of 70%, the percentage of cells exhibiting normal morphology was enhanced by at least 20-fold, and the volume of microvesicles released from red blood cells was reduced by 50% after 35 days of refrigerated storage compared to the values obtained from corresponding samples stored without added phthalate. Similar effects were observed regardless of whether blood was stored in nonplasticized polypropylene or tri-(2-ethylhexyl) trimellitate plasticized polyvinylchloride containers and with DEHP solubilized by a variety of emulsifiers. When 300 micrograms/mL DEHP was added to stored blood containing erythrocytes predominantly in the echinocyte conformation, many of the cells reverted to the normal discoid morphology. The addition of this quantity of DEHP to blood had no significant effect on the course of storage-induced changes in erythrocyte adenosine triphosphate (ATP), 2,3-diphosphoglycerate (2,3-DPG), sodium or potassium concentrations. The data are consistent with the hypothesis that DEHP inhibits the deterioration of the red blood cell membrane that results from the refrigerated storage of whole blood.


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.


Biorheology ◽  
1995 ◽  
Vol 32 (2-3) ◽  
pp. 125-125
Author(s):  
M RAZAVIAN ◽  
M BOYNARD ◽  
R GUILLET ◽  
H MEISELMAN ◽  
Y BEUZARD

2017 ◽  
Vol 114 (16) ◽  
pp. 4225-4230 ◽  
Author(s):  
Marion Koch ◽  
Katherine E. Wright ◽  
Oliver Otto ◽  
Maik Herbig ◽  
Nichole D. Salinas ◽  
...  

Invasion of the red blood cell (RBC) by the Plasmodium parasite defines the start of malaria disease pathogenesis. To date, experimental investigations into invasion have focused predominantly on the role of parasite adhesins or signaling pathways and the identity of binding receptors on the red cell surface. A potential role for signaling pathways within the erythrocyte, which might alter red cell biophysical properties to facilitate invasion, has largely been ignored. The parasite erythrocyte-binding antigen 175 (EBA175), a protein required for entry in most parasite strains, plays a key role by binding to glycophorin A (GPA) on the red cell surface, although the function of this binding interaction is unknown. Here, using real-time deformability cytometry and flicker spectroscopy to define biophysical properties of the erythrocyte, we show that EBA175 binding to GPA leads to an increase in the cytoskeletal tension of the red cell and a reduction in the bending modulus of the cell’s membrane. We isolate the changes in the cytoskeleton and membrane and show that reduction in the bending modulus is directly correlated with parasite invasion efficiency. These data strongly imply that the malaria parasite primes the erythrocyte surface through its binding antigens, altering the biophysical nature of the target cell and thus reducing a critical energy barrier to invasion. This finding would constitute a major change in our concept of malaria parasite invasion, suggesting it is, in fact, a balance between parasite and host cell physical forces working together to facilitate entry.


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