Malaria parasite Plasmodium gallinaceum up-regulates host red blood cell channels.
The properties of the malaria parasite-induced permeability pathways in the host red blood cell have been a major area of interest particularly in the context of whether the pathways are host- or parasite-derived. In the present study, the whole-cell configuration of the patch-clamp technique has been used to show that, compared with normal cells, chicken red blood cells infected by Plasmodium gallinaceum exhibited a 5-40-fold larger membrane conductance, which could be further increased up to 100-fold by raising intracellular Ca(2+) levels. The increased conductance was not due to pathways with novel electrophysiological properties. Rather, the parasite increased the activity of endogenous 24 pS stretch-activated non-selective cationic (NSC) and 62 pS calcium-activated NSC channels, and, in some cases, of endogenous 255 pS anionic channels.
Thomas
S L
SL
Centre National de la Recherche Scientifique, UPR 9042, Station Biologique, Place G. Teissier, 29682 Roscoff Cedex, France. thomas@sb-roscoff.fr
Egée
S
S
Lapaix
F
F
Kaestner
L
L
Staines
H M
HM
Ellory
J C
JC
D000818:Animals; D002645:Chickens; D004594:Electrophysiology; D004912:Erythrocytes / Q000378:metabolism / Q000469:parasitology* / Q000502:physiology; D006790:Host-Parasite Interactions; D007473:Ion Channels / Q000378:metabolism* / Q000502:physiology; D018408:Patch-Clamp Techniques; D010964:Plasmodium gallinaceum / Q000502:physiology*
D007473:Ion Channels