|
|
 Previous Article | Table of Contents | Next Article 
Rigid membranes of Malayan ovalocytes: a likely genetic barrier against
malaria
N Mohandas, LE Lie-Injo, M Friedman and JW Mak
A high frequency of nonhemolytic hereditary ovalocytosis in Malayan
aborigines is thought to result from reduced susceptibility of affected
individuals to malaria. Indeed, Kidson et al. recently showed that
ovalocytes from Melanesians in Papua New Guinea are resistant to infection
in culture by the malarial parasite Plasmodium falciparum. In order to
determine if protection against parasitic invasion in these ovalocytes
might be the result of some altered membrane material property in these
unusual cells, we measured their membrane and cellular deformability
characteristics using an ektacytometer . Ovalocytic red cells were found to
be much less deformable in comparison to normal discoid red cells. Similar
measurements on isolated membrane preparations revealed a marked reduction
in ovalocytic membrane deformability. To produce equal deformation of
ovalocytic and normal membranes, ovalocytes required an 8-10-fold increase
in applied shear stress, indicating that their membrane was capable of
deforming under sufficient stress. To test the possibility that this
increased membrane rigidity might confer resistance to parasitic invasion,
we performed an in vitro invasion assay using Plasmodium falciparum
merozoites and Malayan ovalocytes of varying deformability from seven
different donors. The level of infection of the ovalocytes ranged from 1%
to 35% of that in control cells, and the extent of inhibition appeared to
be closely related to the reduction in membrane deformability. Moreover, we
were able to induce similar resistance to parasitic invasion in
nonovalocytic normal red cells by increasing their membrane rigidity with
graded exposure to a protein crosslinking agent. Our findings suggest that
resistance to parasite invasion of Malayan ovalocytes is the result of a
genetic mutation that causes increased membrane rigidity.
Volume 63,
Issue 6,
pp. 1385-1392,
06/01/1984
Copyright © 1984 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
N. Mohandas and P. G. Gallagher
Red cell membrane: past, present, and future
Blood,
November 15, 2008;
112(10):
3939 - 3948.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Tiffert, V. L. Lew, H. Ginsburg, M. Krugliak, L. Croisille, and N. Mohandas
The hydration state of human red blood cells and their susceptibility to invasion by Plasmodium falciparum
Blood,
June 15, 2005;
105(12):
4853 - 4860.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Cortes, A. Benet, B. M. Cooke, J. W. Barnwell, and J. C. Reeder
Ability of Plasmodium falciparum to invade Southeast Asian ovalocytes varies between parasite lines
Blood,
November 1, 2004;
104(9):
2961 - 2966.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. J. Bennett, N. Mohandas, and R. L. Coppel
Defining the Minimal Domain of the Plasmodium falciparum Protein MESA Involved in the Interaction with the Red Cell Membrane Skeletal Protein 4.1
J. Biol. Chem.,
June 13, 1997;
272(24):
15299 - 15306.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A Che, R. Cherry, L. Bannister, and A. Dluzewski
Aggregation of band 3 in hereditary ovalocytic red blood cell membranes. Electron microscopy and protein rotational diffusion studies
J. Cell Sci.,
January 7, 1993;
105(3):
655 - 660.
[Abstract]
[PDF]
|
|
|
|
|
