Conserved regions from Plasmodium falciparum MSP11 specifically interact with host cells and have a potential role during merozoite invasion of red blood cells

2010 ◽  
Vol 110 (4) ◽  
pp. 882-892 ◽  
Author(s):  
Ana Zuleima Obando-Martinez ◽  
Hernando Curtidor ◽  
Magnolia Vanegas ◽  
Gabriela Arévalo-Pinzón ◽  
Manuel Alfonso Patarroyo ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Potential Role ◽  
Host Cells ◽  
Merozoite Invasion ◽  
Conserved Regions

scholarly journals Identification of Proteins from Plasmodium falciparum That Are Homologous to Reticulocyte Binding Proteins inPlasmodium vivax

2001 ◽  
Vol 69 (2) ◽  
pp. 1084-1092 ◽  
Author(s):  
Tony Triglia ◽  
Jenny Thompson ◽  
Sonia R. Caruana ◽  
Mauro Delorenzi ◽  
Terry Speed ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Molecular Mass ◽  
Blood Cells ◽  
Potential Role ◽  
High Molecular Mass ◽  
In Vitro Growth ◽  
Merozoite Invasion ◽  
Genome Databases

ABSTRACT Plasmodium falciparum infections can be fatal, whileP. vivax infections usually are not. A possible factor involved in the greater virulence of P. falciparum is that this parasite grows in red blood cells (RBCs) of all maturities whereasP. vivax is restricted to growth in reticulocytes, which represent only approximately 1% of total RBCs in the periphery. Two proteins, expressed at the apical end of the invasive merozoite stage from P. vivax, have been implicated in the targeting of reticulocytes for invasion by this parasite. A search of the P. falciparum genome databases has identified genes that are homologous to the P. vivax rbp-1 and -2 genes. Two of these genes are virtually identical over a large region of the 5′ end but are highly divergent at the 3′ end. They encode high-molecular-mass proteins of >300 kDa that are expressed in late schizonts and localized to the apical end of the merozoite. To test a potential role in merozoite invasion of RBCs, we analyzed the ability of these proteins to bind to mature RBCs and reticulocytes. No binding to mature RBCs or cell preparations enriched for reticulocytes was detected. We identified a parasite clone that lacks the gene for one of these proteins, showing that the gene is not required for normal in vitro growth. Antibodies to these proteins can inhibit merozoite invasion of RBCs.

Effect of Different Fractions of Heparin on Plasmodium falciparum Merozoite Invasion of Red Blood Cells in Vitro

1992 ◽  
Vol 46 (5) ◽  
pp. 589-594 ◽  
Author(s):  
Asli Kulane ◽  
Birgitta Wahlin ◽  
Peter Perlmann ◽  
Hans-Peter Ekre ◽  
Lars Rombo ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Merozoite Invasion ◽  
Falciparum Merozoite

Two MSA 2 peptides that bind to human red blood cells are relevant to Plasmodium falciparum merozoite invasion

2000 ◽  
Vol 55 (3) ◽  
pp. 216-223 ◽  
Author(s):  
M. Ocampo ◽  
M. Urquiza ◽  
F. Guzmán ◽  
L.E. Rodriguez ◽  
J. Suarez ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Merozoite Invasion ◽  
Human Red Blood Cells ◽  
Falciparum Merozoite

scholarly journals Reticulocyte Infection Leads to Altered Behaviour, Drug Sensitivity and Host Cell Remodelling by Plasmodium falciparum

2019 ◽  
Author(s):  
Renugah Naidu ◽  
Trang TT Chu ◽  
Jaishree Tripathi ◽  
Yang Hu ◽  
Gowtham Subramanian ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Host Cell ◽  
Blood Cells ◽  
Host Cells ◽  
Differential Sensitivity ◽  
Parasite Development ◽  
Asexual Development ◽  
Disease Manifestation

AbstractPlasmodia are host-specific, both at the organism and cellular levels. During asexual development, Plasmodium spp. infect cells of erythroid lineage, with an overall propensity towards reticulocytes. This applies to even Plasmodium (P.) falciparum, the most common causative agent of human malaria, implications of which remain unexplored. Herein, for the first time, we characterize the developmental stages and features of P. falciparum cultured in vitro in young reticulocytes (CD71+) in comparison to standard normocyte (CD71-) cultures. We demonstrate that there are notable differences in the patterns of invasion, development and sensitivity to potent antimalarials (such as artemisinin and dihydroartemisinin) for parasites residing in CD71+ reticulocytes. Through a transcriptomic approach, we report that P. falciparum parasites are able to sense the host cell environment, and calibrate their metabolic and host cell remodelling pathways through differential gene expression. These results form an exciting avenue on which hitherto unexplored interactions between Plasmodium spp and different stages of host red blood cells could be investigated in the broader contexts of drug resistance, host tropism and zoonosis.Author SummaryParasites causing malaria infect red blood cells for development and proliferation during asexual development. This asexual erythrocytic stage determines higher parasite densities and eventual disease manifestation. Although the most virulent species of Plasmodium infecting humans known as Plasmodium falciparum is able to infect red blood cells of all ages, these parasites show a preference for younger blood cells. Of note, the biochemical and biophysical properties of young and adult red blood cells vary significantly. Herein, we undertook a comparative profiling of invasion process, parasite development and drug response of Plasmoddium falciparum in two host cells: young red blood cells (reticulocytes) and mature red blood cells (normocytes). We demonstrate that P. falciparum infects human reticulocytes with higher affinity and demonstrate differential sensitivity to drugs such as artemisinin while they reside within reticulocytes. Furthermore, we show that P. falciparum is able to detect differences in host environment and adapt to it by changing the expression of genes required for host cell remodelling.

Conserved regions of the Plasmodium falciparum rhoptry-associated protein 3 mediate specific host-pathogen interactions during invasion of red blood cells

Peptides ◽  
2010 ◽  
Vol 31 (12) ◽  
pp. 2165-2172 ◽  
Author(s):  
Jeison García ◽  
Hernando Curtidor ◽  
Magnolia Vanegas ◽  
Gabriela Arévalo-Pinzon ◽  
Manuel A. Patarroyo ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Host Pathogen Interactions ◽  
Conserved Regions ◽  
Specific Host ◽  
Host Pathogen

Ultrastructural observations on the in vitro cytoadherence of Plasmodium falciparum infected red blood cells

1990 ◽  
Vol 48 (3) ◽  
pp. 914-915
Author(s):  
D.J.P. Ferguson ◽  
A.R. Berendt ◽  
J. Tansey ◽  
K. Marsh ◽  
C.I. Newbold
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Umbilical Vein ◽  
Cell Types ◽  
Amelanotic Melanoma ◽  
Cytoplasmic Process ◽  
Umbilical Vein Endothelial Cells

In human malaria, the most serious clinical manifestation is cerebral malaria (CM) due to infection with Plasmodium falciparum. The pathology of CM is thought to relate to the fact that red blood cells containing mature forms of the parasite (PRBC) cytoadhere or sequester to post capillary venules of various tissues including the brain. This in vivo phenomenon has been studied in vitro by examining the cytoadherence of PRBCs to various cell types and purified proteins. To date, three Ijiost receptor molecules have been identified; CD36, ICAM-1 and thrombospondin. The specific changes in the PRBC membrane which mediate cytoadherence are less well understood, but they include the sub-membranous deposition of electron-dense material resulting in surface deformations called knobs. Knobs were thought to be essential for cytoadherence, lput recent work has shown that certain knob-negative (K-) lines can cytoadhere. In the present study, we have used electron microscopy to re-examine the interactions between K+ PRBCs and both C32 amelanotic melanoma cells and human umbilical vein endothelial cells (HUVEC).We confirm previous data demonstrating that C32 cells possess numerous microvilli which adhere to the PRBC, mainly via the knobs (Fig. 1). In contrast, the HUVEC were relatively smooth and the PRBCs appeared partially flattened onto the cell surface (Fig. 2). Furthermore, many of the PRBCs exhibited an invagination of the limiting membrane in the attachment zone, often containing a cytoplasmic process from the endothelial cell (Fig. 2).

Endothelin-1 production by a microvascular endothelial cell line treated with Plasmodium falciparum parasitized red blood cells

2002 ◽  
Vol 103 (s2002) ◽  
pp. 464S-466S ◽  
Author(s):  
Nicoletta BASILICO ◽  
Livianna SPECIALE ◽  
Silvia PARAPINI ◽  
Pasquale FERRANTE ◽  
Donatella TARAMELLI
Keyword(s):  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Red Blood Cells ◽  
Cell Line ◽  
Blood Cells ◽  
Microvascular Endothelial Cell ◽  
Microvascular Endothelium ◽  
Endothelial Cell Line ◽  
Endothelin 1 ◽  
Microvascular Endothelial

In this study, we investigated the production of endothelin 1 (ET-1) by a human microvascular endothelial cell line, HMEC-1, co-cultured with Plasmodium falciparum-parasitized red blood cells (pRBCs). The results indicate that hypoxia increased the basal level of ET-1 production by HMEC-1 cells after 24 or 48h of treatment. However, the co-incubation of HMEC-1 cells with pRBCs, but not with uninfected RBCs, induced a dose-dependent decrease of both constitutive and hypoxia-induced ET-1 production. The inhibition was not due to a decrease in cell viability, as lactate dehydrogenase release remained constant. These results indicate that pRBCs are able to interfere with both the constitutive and stimulated ET-1 release from the microvascular endothelium, thus inducing local modifications of the vascular tone and of the inflammatory response. This could be of relevance in the pathogenesis of the most severe forms of P. falciparum infections, such as cerebral malaria or malaria during pregnancy.

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