The avian malaria parasite Plasmodium gallinaceum causes marked structural changes on the surface of its host erythrocyte

Nagao, Eriko; Arie, Takayuki; Dorward, David W.; Fairhurst, Rick M.; Dvorak, James A.

doi:10.1016/j.jsb.2008.03.005

Cited by 21 publications

(15 citation statements)

References 37 publications

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“…iRBC size and deformabilityknowledge gained from in vivo imaging Plasmodium infection introduces marked structural changes in the erythrocyte membrane that cause cellular distortion and increased rigidity and reduced deformability in iRBC harbouring mature parasites (17,151,152). In agreement with the 150-fold preference of PbA for reticulocytes over normocytes (153)(154)(155)(156)(157)(158)(159)(160)(161), a recent IVM study showed that PbA-infected reticulocytes containing large mature parasites travelled slowly through the narrow capillary lumen, while iRBC harbouring small immature parasites travelled at bloodstream velocity (124).…”

Section: Imaging Ecm Pathogenesis In Small Animal Modelsmentioning

confidence: 99%

Immunobiology of Plasmodium in liver and brain

Frevert

Nacer

2013

Parasite Immunology

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Malaria remains one of the most serious health problems globally, but our understanding of the biology of the parasite and the pathogenesis of severe disease is still limited. Multiple cellular effector mechanisms that mediate parasite elimination from the liver have been described, but how effector cells use classical granule-mediated cytotoxicity to attack infected hepatocytes and how cytokines and chemokines spread via the unique fluid pathways of the liver to reach the parasites over considerable distances remains unknown. Similarly, a wealth of information on cerebral malaria (CM), one of the most severe manifestations of the disease, was gained from post-mortem analyses of human brain and murine disease models, but the cellular processes that ultimately cause disease are not fully understood. Here, we discuss how imaging of the local dynamics of parasite infection and host response as well as consideration of anatomical and physiological features of liver and brain can provide a better understanding of the initial asymptomatic hepatic phase of the infection and the cascade of events leading to CM. Given the increasing drug resistance of both parasite and vector and the unavailability of a protective vaccine, the urgency to reduce the tremendous morbidity and mortality associated with severe malaria is obvious.

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Section: Imaging Ecm Pathogenesis In Small Animal Modelsmentioning

confidence: 99%

Immunobiology of Plasmodium in liver and brain

Frevert

Nacer

2013

Parasite Immunology

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“…For example, infected avian erythrocytes with P. gallinaceum develop furrow-like structures instead of knob-like structures like most Plasmodium spp. (Nagao et al 2008). Avian parasites encounter different immunological pressures from their hosts, which result in different methods of erythrocyte invasion.…”

Section: Discussionmentioning

confidence: 99%

Identification and expression of maebl, an erythrocyte-binding gene, in Plasmodium gallinaceum

et al. 2012

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Avian malaria is of significant ecological importance and serves as a model system to study broad patterns of host switching and host-specificity. The erythrocyte invasion mechanism of the malaria parasite Plasmodium is mediated, in large part, by proteins of the erythrocyte binding-like (ebl) family of genes. However, little is known about how these genes are conserved across different species of Plasmodium, especially those that infect birds. Using bioinformatical methods in conjunction with PCR and genetic sequencing, we identified and annotated one member of the ebl family, maebl (merozoite apical erythrocyte binding ligand) from the chicken parasite Plasmodium gallinaceum. We then detected the expression of maebl in P. gallinaceum by PCR analysis of cDNA isolated from the blood of infected chickens. We found that maebl is a conserved orthologous gene in avian, mammalian, and rodent Plasmodium species. The duplicate extracellular binding domains of MAEBL, responsible for erythrocyte binding, are the most conserved regions. Our combined data corroborate the conservation of maebl throughout the Plasmodium genus, and may help elucidate the mechanisms of erythrocyte invasion in P. gallinaceum and the host specificity of Plasmodium parasites.

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“…These features are uniformly distributed on the cell surface and persist in the remaining cycle with identical density and distribution. The dimensions taken from AFM of this furrow-like structure is around 57.3 nm in width, 7.6 nm in depth, and 225 nm to 750 nm in length (Nagao et al 2007). Studies also showed that malaria-infected avian RBCs (miaRBCs) did not sequester efficiently to microvessels like the one infected by P. falciparum.…”

Section: Introductionmentioning

confidence: 97%

“…Similar to human malaria, the Plasmodium gallinaceum infected avian RBCs loose their oval shape and have modified surface morphology (Nagao et al 2007). P. gallinaceum parasite leaves a visible lesion on the cell surface after invasion, and it remains throughout the asexual erythrocytic stages.…”

Section: Introductionmentioning

confidence: 99%

A microfluidic platform to isolate avian erythrocytes infected with Plasmodium gallinaceum malaria parasites based on surface morphological changes

Hsu

Coleman

et al. 2011

Biomed Microdevices

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This paper reports on a microfluidic platform to isolate and study avian red blood cells (RBCs) infected to various degrees by the malaria parasite Plasmodium gallinaceum. The experimental findings point to the feasibility of using the morphological changes on the surface of the malaria infected avian RBC (miaRBCs) as biomarkers for diagnosis. A glass substrate with a controlled surface roughness was used as part of a polydimethylsiloxane (PDMS) microfluidic channels. When whole-blood samples were introduced into the channels, the miaRBCs would be preferentially slowed and eventually become immobilized on the roughened surface. The surface lesions and furrow-like structures on the miaRBC surfaces offered a markedly higher probability to interact with the roughened substrate and allowed the cells to become imobilized on the surface. The captured miaRBCs were from blood samples at various degrees of infection at 3.2%, 3.9%, 9.1%, 13.4%, 20.1%, 28%, and 37%. It was observed that the miaRBCs could be selectively captured under a wall shear rate between 2.1 to 3.2 s(-1), which was directly proportional to the flow rate through the channels. This capture rate could be improved by increasing the channel length and finer flow control. It was also found that a roughened glass substrate with ten-point-height larger than the depth of surface lesions and furrow-like structures of miaRBCs showed a substantial enhancement on the number of immobilized infected RBCs. These findings indicated that surface morphologies, including surface lesions and furrow-like structures, can serve as an alternative biomarker for malaria diagnosis.

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The avian malaria parasite Plasmodium gallinaceum causes marked structural changes on the surface of its host erythrocyte

Cited by 21 publications

References 37 publications

Immunobiology of Plasmodium in liver and brain

Immunobiology of Plasmodium in liver and brain

Identification and expression of maebl, an erythrocyte-binding gene, in Plasmodium gallinaceum

A microfluidic platform to isolate avian erythrocytes infected with Plasmodium gallinaceum malaria parasites based on surface morphological changes

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