Malaria parasite <i>Plasmodium gallinaceum</i> up‐regulates host red blood cell channels

Thomas, Serge; Egée, Stéphane; Lapaix, Franck; Kaestner, Lars; Staines, Henry M.; Ellory, J. Clive

doi:10.1016/s0014-5793(01)02579-0

Cited by 32 publications

(15 citation statements)

References 21 publications

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“…The present study showed significant hemolysis of infected and oxidized cells in NaCl solution, suggesting the entry of NaCl which requires the operation of Na + ‐permeable cation channels in parallel to the Cl − channels. A low non‐selective cation conductance has been demonstrated to be activated in non‐infected human erythrocytes by oxidative stress (Duranton et al ., 2002), and increased activity of non‐selective cation channels has indeed been observed in Plasmodium ‐infected human (Desai et al ., 1996) and chicken erythrocytes (Thomas et al ., 2001).…”

Section: Discussionsupporting

confidence: 89%

Plasmodium falciparum activates endogenous Cl- channels of human erythrocytes by membrane oxidation

et al. 2002

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Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection‐induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole‐cell patch–clamp and hemolysis experiments were performed to define properties of the NPP. Parasitized but not control erythrocytes constitutively expressed two types of anion conductances, differing in voltage dependence and sensitivity to inhibitors. In addition, infected but not control cells hemolyzed in isosmotic sorbitol solution. Both conduct ances and hemolysis of infected cells were inhibited by reducing agents. Conversely, oxidation induced identical conductances and hemolysis in non‐infected erythrocytes. In conclusion, P.falciparum activates endogenous erythrocyte channels by applying oxidative stress to the host cell membrane.

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Section: Discussionsupporting

confidence: 89%

Plasmodium falciparum activates endogenous Cl- channels of human erythrocytes by membrane oxidation

et al. 2002

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“…Ca 2+ signalling may transform the RBC into an active contributor to thrombosis; even if the contribution is small, it might be globally or locally relevant when occurring on top of pre-existing pathologies. Furthermore, there is growing clinical evidence in support of Ca 2+ -associated pro-thrombotic activity of RBCs in diseases such as β-thalassemia [31], [70], sickle cell disease [71], [72] or malaria [73], [74].…”

Section: Discussionmentioning

confidence: 99%

Morphologically Homogeneous Red Blood Cells Present a Heterogeneous Response to Hormonal Stimulation

et al. 2013

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Red blood cells (RBCs) are among the most intensively studied cells in natural history, elucidating numerous principles and ground-breaking knowledge in cell biology. Morphologically, RBCs are largely homogeneous, and most of the functional studies have been performed on large populations of cells, masking putative cellular variations. We studied human and mouse RBCs by live-cell video imaging, which allowed single cells to be followed over time. In particular we analysed functional responses to hormonal stimulation with lysophosphatidic acid (LPA), a signalling molecule occurring in blood plasma, with the Ca2+ sensor Fluo-4. Additionally, we developed an approach for analysing the Ca2+ responses of RBCs that allowed the quantitative characterization of single-cell signals. In RBCs, the LPA-induced Ca2+ influx showed substantial diversity in both kinetics and amplitude. Also the age-classification was determined for each particular RBC and consecutively analysed. While reticulocytes lack a Ca2+ response to LPA stimulation, old RBCs approaching clearance generated robust LPA-induced signals, which still displayed broad heterogeneity. Observing phospatidylserine exposure as an effector mechanism of intracellular Ca2+ revealed an even increased heterogeneity of RBC responses. The functional diversity of RBCs needs to be taken into account in future studies, which will increasingly require single-cell analysis approaches. The identified heterogeneity in RBC responses is important for the basic understanding of RBC signalling and their contribution to numerous diseases, especially with respect to Ca2+ influx and the associated pro-thrombotic activity.

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“…in the presence of serum), outwardly rectifying currents have been measured in both P. falciparum and P. berghei ‐infected erythocytes (Huber et al ., 2004; Staines et al ., 2006) but these again have different characteristics to those measured here, having time‐dependent current inactivation at negative potentials and none at high positive potentials. In addition, chicken erythrocytes infected with P. gallinaceum , although having altered electroneutral and electrogenic solute transport, do not activate VRACs (Thomas et al ., 2001; Staines et al ., 2002), even though cell swelling does induce them (note that, unlike avian erythrocytes, mammalian erythrocytes are some of the few cell types that do not activate VRACs upon cell swelling).…”

Section: Discussionmentioning

confidence: 99%

Plasmodium berghei-infection induces volume-regulated anion channel-like activity in human hepatoma cells

Prudêncio

Derbyshire

Marques

et al. 2009

Cellular Microbiology

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Parasite infection can lead to alterations in the permeability of host plasma membranes. Presented here is the first demonstration that this phenomenon occurs in Plasmodium-infected liver cells. Using the whole-cell patch-clamp technique, volume-regulated anion channel (VRAC) activity was characterized in Huh-7 cells (a human hepatoma cell line) before and after infection with Plasmodium berghei. Consistent with the presence of VRACs, hypotonic bath solution induced large ion currents in Huh-7 cells that rectified outwardly, reversed close to the equilibrium potential for Cl- and were inhibited by tamoxifen, clomiphene, mefloquine and 5-nitro-2, 3-(phenylpropylamino)-benzoic acid (NPPB), with IC50 values of 4 ± 1, 4 ± 2, 2 ± 1 and 52 ± 12 μM respectively. In isotonic conditions, initial current recordings measured in uninfected and immature (24 h post invasion) parasite-infected Huh-7 cells were similar (with conductances of 14 ± 3 versus 19 ± 5 pS/pF). However, in mature (48–72 h post invasion) parasite-infected Huh-7 cells there was a sevenfold increase in currents (with a conductance of 98 ± 16 pS/pF). The elevated currents observed in the latter are consistent with VRAC-like activity and the possible reasons for their activation are discussed.

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

Cited by 32 publications

References 21 publications

Plasmodium falciparum activates endogenous Cl- channels of human erythrocytes by membrane oxidation

Plasmodium falciparum activates endogenous Cl- channels of human erythrocytes by membrane oxidation

Morphologically Homogeneous Red Blood Cells Present a Heterogeneous Response to Hormonal Stimulation

Plasmodium berghei-infection induces volume-regulated anion channel-like activity in human hepatoma cells

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