Plasmodium falciparum is able to invade erythrocytes through a trypsin-resistant pathway independent of glycophorin B
(2003) In Infection and Immunity 71(12). p.6742-6746- Abstract
- Plasmodium falciparum invades erythrocytes through multiple ligand-receptor interactions, with redundancies in each pathway. One such alternate pathway is the trypsin-resistant pathway that enables P. falciparum to invade trypsin-treated erythrocytes. Previous studies have shown that this trypsin-resistant pathway is dependent on glycophorin B, as P. falciparum strains invade trypsin-digested glycophorin B-deficient erythrocytes at a highly reduced efficiency. Furthermore, in a recent study, the P. falciparum 7G8 strain did not invade glycophorin B-deficient erythrocytes, a finding that was not confirmed in the present study. To analyze the degree of dependence on glycophorin B for invasion by P. falciparum through the trypsin-resistant... (More)
- Plasmodium falciparum invades erythrocytes through multiple ligand-receptor interactions, with redundancies in each pathway. One such alternate pathway is the trypsin-resistant pathway that enables P. falciparum to invade trypsin-treated erythrocytes. Previous studies have shown that this trypsin-resistant pathway is dependent on glycophorin B, as P. falciparum strains invade trypsin-digested glycophorin B-deficient erythrocytes at a highly reduced efficiency. Furthermore, in a recent study, the P. falciparum 7G8 strain did not invade glycophorin B-deficient erythrocytes, a finding that was not confirmed in the present study. To analyze the degree of dependence on glycophorin B for invasion by P. falciparum through the trypsin-resistant pathway, we have studied the invasion phenotypes of five parasite strains, 3D7, HB3, Dd2, 7G8, and Indochina I, on trypsin-treated normal and glycophorin B-deficient erythrocytes. Invasion was variably reduced in glycophorin B-deficient erythrocytes. Four strains, 3D7, HB3, Dd2, and Indochina I, invaded trypsin-treated erythrocytes, while invasion by the 7G8 strain was reduced by 90%. Among the four strains, invasion by 3D7, HB3, and Dd2 of trypsin-digested glycophorin B-deficient erythrocytes was further reduced. However, Indochina I invaded trypsin-digested glycophorin B-deficient erythrocytes at the same efficiency as its invasion of trypsin-digested normal erythrocytes. This strongly suggests that the Indochina I strain of P. falciparum is not dependent on glycophorin B to invade through a trypsin-resistant pathway as are the strains 3D7, HB3, and Dd2. Thus, P. falciparum is able to invade erythrocytes through a glycophorin B-independent, trypsin-resistant pathway. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1126496
- author
- Gaur, Deepak ; Storry, Jill LU ; Reid, Marion E ; Barnwell, John W and Miller, Louis H
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Infection and Immunity
- volume
- 71
- issue
- 12
- pages
- 6742 - 6746
- publisher
- American Society for Microbiology
- external identifiers
-
- pmid:14638759
- scopus:0345714791
- ISSN
- 1098-5522
- DOI
- 10.1128/IAI.71.12.6742-6746.2003
- language
- English
- LU publication?
- no
- id
- 7a52b514-fc4a-469f-8ece-c93fa55a1129 (old id 1126496)
- date added to LUP
- 2016-04-01 11:48:39
- date last changed
- 2025-04-04 13:59:15
@article{7a52b514-fc4a-469f-8ece-c93fa55a1129,
abstract = {{Plasmodium falciparum invades erythrocytes through multiple ligand-receptor interactions, with redundancies in each pathway. One such alternate pathway is the trypsin-resistant pathway that enables P. falciparum to invade trypsin-treated erythrocytes. Previous studies have shown that this trypsin-resistant pathway is dependent on glycophorin B, as P. falciparum strains invade trypsin-digested glycophorin B-deficient erythrocytes at a highly reduced efficiency. Furthermore, in a recent study, the P. falciparum 7G8 strain did not invade glycophorin B-deficient erythrocytes, a finding that was not confirmed in the present study. To analyze the degree of dependence on glycophorin B for invasion by P. falciparum through the trypsin-resistant pathway, we have studied the invasion phenotypes of five parasite strains, 3D7, HB3, Dd2, 7G8, and Indochina I, on trypsin-treated normal and glycophorin B-deficient erythrocytes. Invasion was variably reduced in glycophorin B-deficient erythrocytes. Four strains, 3D7, HB3, Dd2, and Indochina I, invaded trypsin-treated erythrocytes, while invasion by the 7G8 strain was reduced by 90%. Among the four strains, invasion by 3D7, HB3, and Dd2 of trypsin-digested glycophorin B-deficient erythrocytes was further reduced. However, Indochina I invaded trypsin-digested glycophorin B-deficient erythrocytes at the same efficiency as its invasion of trypsin-digested normal erythrocytes. This strongly suggests that the Indochina I strain of P. falciparum is not dependent on glycophorin B to invade through a trypsin-resistant pathway as are the strains 3D7, HB3, and Dd2. Thus, P. falciparum is able to invade erythrocytes through a glycophorin B-independent, trypsin-resistant pathway.}},
author = {{Gaur, Deepak and Storry, Jill and Reid, Marion E and Barnwell, John W and Miller, Louis H}},
issn = {{1098-5522}},
language = {{eng}},
number = {{12}},
pages = {{6742--6746}},
publisher = {{American Society for Microbiology}},
series = {{Infection and Immunity}},
title = {{Plasmodium falciparum is able to invade erythrocytes through a trypsin-resistant pathway independent of glycophorin B}},
url = {{http://dx.doi.org/10.1128/IAI.71.12.6742-6746.2003}},
doi = {{10.1128/IAI.71.12.6742-6746.2003}},
volume = {{71}},
year = {{2003}},
}