Malaria parasite Plasmodium gallinaceum up‐regulates host red blood cell channels

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Abstract
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 Ca2+ 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.