Mechanical response of human red blood cells in health and disease: Some structure-property-function relationships

2006 ◽  
Vol 21 (8) ◽  
pp. 1871-1877 ◽  
Author(s):  
S. Suresh

Aspects of mechanical deformability and biorheology of the human red blood cell are known to play a pivotal role in influencing organ function as well as states of overall health and disease. In this article, consequences of alterations to the membrane and cytoskeletal molecular structure of the human red blood cell are considered in the context of an infectious disease,Plasmodium falciparummalaria, and several hereditary hemolytic disorders: spherocytosis, elliptocytosis, and sickle cell anemia. In each of these cases, the effects of altered cell shape or molecular structure on cell elasticity, motility, and biorheology are examined. These examples are used to gain broad perspectives on the connections among cell and subcellular structure, properties, and disease at the intersections of engineering, biology, and medicine.

2004 ◽  
Vol 844 ◽  
Author(s):  
John P. Mills ◽  
Lan Qie ◽  
Ming Dao ◽  
Kevin S. W. Tan ◽  
Chwee Teck Lim ◽  
...  

ABSTRACTPrior work involving either aspiration of infected cells into micropipette under suction pressure or deformation in laminar shear flow revealed that the malaria parasitePlasmodium (P.) falciparumcould result in significant stiffening of infected human red blood cells (RBCs). In this paper, we present optical tweezers studies of progressive changes to nonlinear mechanical response of infected RBCs at different developmental stages ofP. falciparum.From early ring stage to late trophozoite and schizont stages, up to an order of magnitude increase in shear modulus was found under controlled mechanical loading by combining experiments with three-dimensional computational simulations. These results provide novel approaches to study changes in mechanical deformability in the advanced stages of parasite development in the erythrocyte, and suggest a significantly greater stiffening of the red blood cell due toP. falciparuminvasion than that considered from previous studies.


Soft Matter ◽  
2020 ◽  
Vol 16 (26) ◽  
pp. 6191-6205 ◽  
Author(s):  
Fabio Guglietta ◽  
Marek Behr ◽  
Luca Biferale ◽  
Giacomo Falcucci ◽  
Mauro Sbragaglia

Computational Fluid Dynamics is currently used to design and improve the hydraulic properties of biomedical devices, wherein the large scale blood circulation needs to be simulated by accounting for the mechanical response of RBCs at the mesoscale.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Sebastian Himbert ◽  
Richard J. Alsop ◽  
Markus Rose ◽  
Laura Hertz ◽  
Alexander Dhaliwal ◽  
...  

2004 ◽  
Vol 6 (6) ◽  
pp. 992-999
Author(s):  
Jack H. Crawford ◽  
Balu K. Chacko ◽  
Christopher G. Kevil ◽  
Rakesh P. Patel

Blood ◽  
1992 ◽  
Vol 80 (3) ◽  
pp. 801-808 ◽  
Author(s):  
F Turrini ◽  
H Ginsburg ◽  
F Bussolino ◽  
GP Pescarmona ◽  
MV Serra ◽  
...  

Abstract The stage-dependent phagocytosis of Plasmodium falciparum-infected erythrocytes (IRBC) opsonized with nonimmune serum has been investigated. An average of 2.9 red blood cell (RBC) harboring ring- forms (RIRBC) and 7.5 RBC infected with trophozoites (TIRBC) or schizonts (SIRBC) were ingested per monocyte, in comparison with 0.8 noninfected RBC (NRBC) or 5 RBC oxidatively damaged with diamide. Abrogation of generation of complement component C3b or blockage of its binding to the phagocyte inhibited phagocytosis of RIRBC by 78% to 95% and of TIRBC by 25% to 50%. Blockage of immunoglobulin G (IgG) binding reduced phagocytosis of both RIRBC and TIRBC nonsignificantly by 14%. Preincubation of monocytes with phosphatidylserine (PS)-containing liposomes reduced phagocytosis of TIRBC by 22%, but had little effect on RIRBC. Residual, noncomplement, non-IgG-, and non-PS-dependent phagocytosis amounted to 6% to 18% of total phagocytosis in RIRBC and TIRBC, respectively. RIRBC bound 2.5 times more protein A and 3.1 times more anti-C3c (a stable derivative of C3b) antibodies, and TIRBC bound 20 times more protein A and 6.8 times more anti-C3c antibodies than NRBC. Phagocytosis of oxidatively damaged RBC and RIRBC are similar, whereas a higher portion of phagocytosis appears to be noncomplement- dependent and PS-suppressible in TIRBC. It is concluded that RIRBC generate recognition signals similar to those present in oxidatively damaged or senescent RBC. Extensive membrane modifications in TIRBC produce additional, hitherto undefined signals that induce much higher and qualitatively distinct phagocytosis.


2007 ◽  
Vol 293 (2) ◽  
pp. C597-C605 ◽  
Author(s):  
Marina Puig-de-Morales-Marinkovic ◽  
Kevin T. Turner ◽  
James P. Butler ◽  
Jeffrey J. Fredberg ◽  
Subra Suresh

We report here the first measurements of the complex modulus of the isolated red blood cell (RBC). Because the RBC is often larger than capillary diameter, important determinants of microcirculatory function are RBC deformability and its changes with pathologies, such as sickle cell disease and malaria. A functionalized ferrimagnetic microbead was attached to the membrane of healthy RBC and then subjected to an oscillatory magnetic field. The resulting torque caused cell deformation. From the oscillatory forcing and resulting bead motions, which were tracked optically, we computed elastic and frictional moduli, g′ and g‴, respectively, from 0.1 to 100 Hz. The g′ was nearly frequency independent and dominated the response at all but the highest frequencies measured. Over three frequency decades, g‴ increased as a power law with an exponent of 0.64, a result not predicted by any simple model. These data suggest that RBC relaxation times that have been reported previously, and any models that rest upon them, are artifactual; the artifact, we suggest, arises from forcing to an exponential fit data of limited temporal duration. A linear range of response was observed, but, as forcing amplitude increased, nonlinearities became clearly apparent. A finite element model suggests that membrane bending was localized to the vicinity of the bead and dominated membrane shear. While the mechanisms accounting for these RBC dynamics remain unclear, methods described here establish new avenues for the exploration of connections among the mechanical, chemical, and biological characteristics of the RBC in health and disease.


1989 ◽  
Vol 93 (2) ◽  
pp. 321-342 ◽  
Author(s):  
P A King ◽  
R B Gunn

Na- and Cl-dependent glycine transport was investigated in human red blood cells. The effects of the carrier substrates (Na, Cl, and glycine) on the glycine transport kinetics were studied with the goal of learning more about the mechanism of transport. The K1/2-gly was 100 microM and the Vmax-gly was 109 mumol/kg Hb.h. When cis Na was lowered (50 mM) the K1/2-gly increased and the Vmax-gly decreased, which was consistent with a preferred order of rapid equilibrium loading of glycine before Na. Na-dependent glycine influx as a function of Na concentration was sigmoidal, and direct measurement of glycine and Na uptake indicated a stoichiometry of 2 Na:1 glycine transported. The sigmoidal response of glycine influx to Na concentration was best fit by a model with ordered binding of Na, the first Na with a high K1/2 (greater than 250 mM), and the second Na with a low K1/2 (less than 10.3 mM). In the presence of low Cl (cis and trans 5 mM), the K1/2-gly increased and the Vmax-gly increased. The Cl dependence displayed Michaelis-Menten kinetics with a K1/2-Cl of 9.5 mM. At low Cl (5 mM Cl balanced with NO3), the glycine influx as a function of Na showed the same stoichiometry and Vmax-Na but a decreased affinity of the carrier for Na. These data suggested that Cl binds to the carrier before Na. Experiments comparing influx and efflux rates of transport using red blood cell ghosts indicated a functional asymmetry of the transporter. Under the same gradient conditions, Na- and Cl-dependent glycine transport functioned in both directions across the membrane but rates of efflux were 50% greater than rates of influx. In addition, the presence of trans substrates modified influx and efflux differently. Trans glycine largely inhibited glycine efflux in the absence or presence of trans Na; trans Na largely inhibited glycine influx and this inhibition was partially reversed when trans glycine was also present. A model for the binding of these substrates to the outward-facing carrier is presented.


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