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Separation of Plasmodium falciparum Late Stage-infected Erythrocytes by Magnetic Means
Published on: March 2, 2013
Studying the rigidity of red blood cells induced by Plasmodium falciparum infection
Apurba Paul1, Ghania Ramdani2, Utpal Tatu3
1Department of Physics, Indian Institute of Science, Bangalore, 560012, India.
Abstract:
We study the effect of different chemical moieties on the rigidity of red blood cells (RBCs) induced by Plasmodium falciparum infection, and the bystander effect previously found. The infected cells are obtained from a culture of parasite-infected RBCs grown in the laboratory. The rigidity of RBCs is measured by looking at the Brownian fluctuations of individual cells in an optical-tweezers trap. The results point towards increased intracellular cyclic adenosine monophosphate (cAMP) levels as being responsible for the increase in rigidity.
Insights
Plasmodium falciparum infection increases red blood cell rigidity. This study found that elevated cyclic adenosine monophosphate (cAMP) levels are responsible for this change in infected cells.
Area of Science:
- Biophysics
- Cell Biology
- Parasitology
Background:
- Plasmodium falciparum infection alters red blood cell (RBC) properties.
- A bystander effect has been observed in uninfected RBCs near infected cells.
- RBC rigidity changes are critical in understanding disease progression.
Purpose of the Study:
- To investigate the impact of chemical moieties on RBC rigidity during P. falciparum infection.
- To elucidate the mechanism behind the increased RBC rigidity.
- To explore the role of intracellular signaling in altered RBC mechanics.
Main Methods:
- Culturing Plasmodium falciparum-infected RBCs in vitro.
- Measuring RBC rigidity using optical-tweezers to analyze Brownian fluctuations.
- Quantifying intracellular cyclic adenosine monophosphate (cAMP) levels.
Main Results:
- Infected RBCs exhibit increased rigidity compared to uninfected cells.
- Elevated intracellular cAMP levels were observed in infected RBCs.
- A correlation was established between increased cAMP and enhanced RBC rigidity.
Conclusions:
- Increased intracellular cAMP is a key mediator of RBC rigidity in P. falciparum-infected cells.
- Understanding these mechanical changes can inform therapeutic strategies.
- Further research into chemical moieties affecting RBCs is warranted.
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