Life cycle-dependent cytoskeletal modifications in Plasmodium falciparum infected erythrocytes

• Published in: PloS one 2013-04, Vol.8 (4), p.e61170-e61170
• Main Authors: Shi, Hui, Liu, Zhuo, Li, Ang, Yin, Jing, Chong, Alvin G L, Tan, Kevin S W, Zhang, Yong, Lim, Chwee Teck
• Format: Article
• Language: English
• Subjects: Atomic force microscopy; Bioengineering; Biology; Biomechanics; Blood; Cytoskeletal Proteins - chemistry; Cytoskeletal Proteins - metabolism; Cytoskeleton; Deformability; Deformation; Erythrocyte Deformability; Erythrocyte Membrane - chemistry; Erythrocyte Membrane - parasitology; Erythrocyte Membrane - ultrastructure; Erythrocytes; Erythrocytes - chemistry; Erythrocytes - parasitology; Erythrocytes - ultrastructure; Formability; Health aspects; Humans; Infection; Infections; Knobs; Laboratories; Life cycle engineering; Life cycles; Malaria; Medical imaging; Medicine; Membrane proteins; Microscopy; Microscopy, Atomic Force; Morphology; Parasites; Parasitology; Pathogenesis; Plasmodium; Plasmodium falciparum; Plasmodium falciparum - physiology; Protein Multimerization; Proteins; Quantum dots; Schizonts - physiology; Spectrin; Trophozoites - physiology; Vector-borne diseases
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0061170

Plasmodium falciparum infection of human erythrocytes is known to result in the modification of the host cell cytoskeleton by parasite-coded proteins. However, such modifications and corresponding implications in malaria pathogenesis have not been fully explored. Here, we probed the gradual modification of infected erythrocyte cytoskeleton with advancing stages of infection using atomic force microscopy (AFM). We reported a novel strategy to derive accurate and quantitative information on the knob structures and their connections with the spectrin network by performing AFM-based imaging analysis of the cytoplasmic surface of infected erythrocytes. Significant changes on the red cell cytoskeleton were observed from the expansion of spectrin network mesh size, extension of spectrin tetramers and the decrease of spectrin abundance with advancing stages of infection. The spectrin network appeared to aggregate around knobs but also appeared sparser at non-knob areas as the parasite matured. This dramatic modification of the erythrocyte skeleton during the advancing stage of malaria infection could contribute to the loss of deformability of the infected erythrocyte.