Studies on the Role of Antibodies Against Sporozoites in Plasmodium Berghei Malaria

2015 ◽  
pp. 104-108
Author(s):  
J. Golenser ◽  
J. P. Verhave ◽  
J. de Valk ◽  
J. Heeren ◽  
J. H. E.Th. Meuwissen
Keyword(s):  
Plasmodium Berghei

Intracellular calcium levels in the Plasmodium berghei ookinete

Parasitology ◽  
2008 ◽  
Vol 135 (12) ◽  
pp. 1355-1362 ◽  
Author(s):  
I. SIDÉN-KIAMOS ◽  
C. LOUIS
Keyword(s):  
Intracellular Calcium ◽  
Plasmodium Berghei ◽  
Calcium Concentration ◽  
Insect Cells ◽  
Ionophore A23187 ◽  
Rodent Malaria Parasite ◽  
Calcium Indicators ◽  
Intracellular Ca

SUMMARYOokinetes are the motile and invasive stages of Plasmodium parasites in the mosquito host. Here we explore the role of intracellular Ca2+ in ookinete survival and motility as well as in the formation of oocysts in vitro in the rodent malaria parasite Plasmodium berghei. Treatment with the Ca2+ ionophore A23187 induced death of the parasite, an effect that could be prevented if the ookinetes were co-incubated with insect cells before incubation with the ionophore. Treatment with the intracellular calcium chelator BAPTA/AM resulted in increased formation of oocysts in vitro. Calcium imaging in the ookinete using fluorescent calcium indicators revealed that the purified ookinetes have an intracellular calcium concentration in the range of 100 nm. Intracellular calcium levels decreased substantially when the ookinetes were incubated with insect cells and their motility was concomitantly increased. Our results suggest a pleiotropic role for intracellular calcium in the ookinete.

scholarly journals Protection against malaria in mice is induced by blood stage–arresting histamine-releasing factor (HRF)–deficient parasites

2016 ◽  
Vol 213 (8) ◽  
pp. 1419-1428 ◽  
Author(s):  
Claudia Demarta-Gatsi ◽  
Leanna Smith ◽  
Sabine Thiberge ◽  
Roger Peronet ◽  
Pierre-Henri Commere ◽  
...  
Keyword(s):  
Immune Responses ◽  
Plasmodium Berghei ◽  
Blood Cells ◽  
Housekeeping Genes ◽  
Blood Stage ◽  
Parasite Development ◽  
Rodent Models ◽  
Cell Responses ◽  
Blood Stage Malaria

Although most vaccines against blood stage malaria in development today use subunit preparations, live attenuated parasites confer significantly broader and more lasting protection. In recent years, Plasmodium genetically attenuated parasites (GAPs) have been generated in rodent models that cause self-resolving blood stage infections and induce strong protection. All such GAPs generated so far bear mutations in housekeeping genes important for parasite development in red blood cells. In this study, using a Plasmodium berghei model compatible with tracking anti–blood stage immune responses over time, we report a novel blood stage GAP that lacks a secreted factor related to histamine-releasing factor (HRF). Lack of HRF causes an IL-6 increase, which boosts T and B cell responses to resolve infection and leave a cross-stage, cross-species, and lasting immunity. Mutant-induced protection involves a combination of antiparasite IgG2c antibodies and FcγR+ CD11b+ cell phagocytes, especially neutrophils, which are sufficient to confer protection. This immune-boosting GAP highlights an important role of opsonized parasite-mediated phagocytosis, which may be central to protection induced by all self-resolving blood stage GAP infections.

scholarly journals Interferon and Interferon Inducers in Protozoal Infections

1970 ◽  
Vol 56 (1) ◽  
pp. 227-237 ◽  
Author(s):  
Rene I. Jahiel
Keyword(s):  
Protective Effect ◽  
Host Cell ◽  
Plasmodium Berghei ◽  
Interferon Inducers ◽  
Intracellular Parasites ◽  
As Species ◽  
Parasite Relationship ◽  
Long Range Planning ◽  
Relationship Of

Several interferon inducers (Newcastle disease virus, statolon, and poly rI:poly rC) as well as exogenous mouse interferon protect mice from sporozoite-induced Plasmodium berghei malaria, as long as they are administered before the end of the preerythrocytic phase of development of the parasite. The protective effect of the interferon inducers was related to their interferon-inducing effect; the protective effect of the interferon preparations was related to the interferon titer of the preparations, and it exhibited other attributes of interferon such as species specificity. In contrast to sporozoite-induced infection, blood forms-induced P. berghei malaria was only weakly susceptible to the protective effect of interferon inducers. This difference may provide an approach to study the mechanism of protection. The growth in cell cultures of another intracellular protozoon, Toxoplasma gondii, is also inhibited by interferon (22). The fact that P. berghei and T. gondii (as well as another group of intracellular parasites susceptible to interferon, the Chlamydia) have their own ribosomes raises questions, concerning the role of host cell ribosomes in the host cell-parasite relationship of these intracellular parasites and in the mechanism of interferon action against them, that can be approached experimentally. The possibility of therapeutic or prophylactic application of interferon or of its inducers to certain protozoal diseases of man and of other animals is still remote, but it has to be considered for long range planning.

Immunity to an attenuated variant ofPlasmodium berghei: role of some non-specific factors

Parasitology ◽  
1985 ◽  
Vol 91 (2) ◽  
pp. 263-272 ◽  
Author(s):  
Seiji waki ◽  
Shushke Nakazawa ◽  
Janice Taverne ◽  
G. A. T. Targett ◽  
J. H. L. Playfair
Keyword(s):  
Plasmodium Berghei ◽  
Tumour Necrosis ◽  
Nk Cell ◽  
Cell Activity ◽  
Nk Cell Activity ◽  
Parasite Number ◽  
Early Peak ◽  
Specific Factors ◽  
Increased Susceptibility

Plasmodium bergheiXAT, an attenuated variant of lethalP. berghei, causes a resolving infection in Balb/c mice from which they recover in about 3 weeks. The parasitaemia displays an early peak at about 5 days, followed by a steep drop in parasite number associated with the appearance of degenerating forms inside mature erythrocytes; the parasites remaining are inside reticulocytes. By contrast, no degenerating parasites were seen in infections caused by the virulent parent, which was mainly confined to mature erythrocytes. However,P. bergheiXAT was no more sensitive to reactive O2metabolites, generated by alloxan, or to tumour necrosis serum, than its virulent parent. Furthermore, its early drop in parasitaemia was unaffected by silica. The drop still occurred in the absence of T cells, although the infection was then ultimately lethal, and it was not mediated by NK cells since it occurred in nude mice treated with anti-asialo GM1 serum to abolish NK cell activity. However, it was absent in splenectomized mice, in whichP. bergheiXAT infection was lethal. Thus, the attenuation ofP. bergheiXAT infection is not due to increased susceptibility to some of the agents thought to cause parasite destruction, but to some other mechanism in which the spleen is involved.

scholarly journals Genetic alteration of ferredoxin NADP+-reductase or cysteine desulfurase in piperaquine-resistant Plasmodium berghei restores susceptibility to lumefantrine and abolishes the impact of probenecid, verapamil, and cyproheptadine

2019 ◽  
Author(s):  
Fagdéba David Bara ◽  
Loise Ndung’u ◽  
Noah Machuki Onchieku ◽  
Beatrice Irungu ◽  
Simplice Damintoti Karou ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei ◽  
Malaria Parasite ◽  
Drug Action ◽  
Cysteine Desulfurase ◽  
Human Malaria Parasite ◽  
Human Malaria ◽  
Essential Components ◽  
The Impact

AbstractChemotherapy remains central in the control of malaria; however, resistance has consistently thwarted these efforts. Currently, lumefantrine (LM), and piperaquine (PQ) drugs, are essential components in the mainstay artemisinin-based therapies used for the treatment of malaria globally. Using LM and PQ-resistant Plasmodium berghei, we measured the effect of known chemosensitizers: probenecid, verapamil, or cyproheptadine on the activity of LM or PQ. Using PlasmoGEM vectors, we then evaluated the impact of deleting cysteine desulfurase (SufS) or over-expressing Ferredoxin NADP+ reductase (FNR), genes that mediate drug action. Our data showed that, only cyproheptadine at 5mgkg−1 restored LM activity by above 65% against the LM-resistant parasites (LMR) but failed to reinstate PQ activity against the PQ-resistant parasites (PQR). Whereas the PQR had lost significant susceptibility to LM, the three chemosensitizers; cyproheptadine, probenecid, and verapamil, restored LM potency against the PQR by above 70%, 60%, and 55% respectively. We thus focused on LM resistance in PQR. Deletion of the SufS or overexpression of the FNR genes in the PQR abolished the impact of the chemosensitizers on the LM activity, and restored the susceptibility of the PQR parasites to LM. Taken together, we demonstrate the association between SufS or FNR genes with the action of LM and chemosensitizers in PQR parasites. There is, however, need to interrogate the impact of the chemosensitizers and the role of SufS or FNR genes on LM action in the human malaria parasite, Plasmodium falciparum.

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