scholarly journals Liposome-Mediated Immunosuppression Plays an Instrumental Role in the Development of “Humanized Mouse” to Study Plasmodium falciparum

Liposomes ◽  
2017 ◽  
Author(s):  
Kunjal Agrawal ◽  
Vishwa Vyas ◽  
Yamnah Hafeji ◽  
Rajeev K. Tyagi
Keyword(s):  
Plasmodium Falciparum ◽  
Humanized Mouse ◽  
Instrumental Role

Identification, Characterization, and Optimization of 2,8-Disubstituted-1,5-naphthyridines as Novel Plasmodium falciparum Phosphatidylinositol-4-kinase Inhibitors with in Vivo Efficacy in a Humanized Mouse Model of Malaria

2018 ◽  
Vol 61 (13) ◽  
pp. 5692-5703 ◽  
Author(s):  
Nishanth Kandepedu ◽  
Diego Gonzàlez Cabrera ◽  
Srinivas Eedubilli ◽  
Dale Taylor ◽  
Christel Brunschwig ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Mouse Model ◽  
Kinase Inhibitors ◽  
Humanized Mouse ◽  
Humanized Mouse Model ◽  
In Vivo Efficacy ◽  
Phosphatidylinositol 4

scholarly journals Plasmodium falciparum genetic crosses in a humanized mouse model

2015 ◽  
Vol 12 (7) ◽  
pp. 631-633 ◽  
Author(s):  
Ashley M Vaughan ◽  
Richard S Pinapati ◽  
Ian H Cheeseman ◽  
Nelly Camargo ◽  
Matthew Fishbaugher ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Mouse Model ◽  
Humanized Mouse ◽  
Humanized Mouse Model ◽  
Genetic Crosses

scholarly journals A humanized mouse model for sequestration of Plasmodium falciparum sexual stages and in vivo evaluation of gametocytidal drugs

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yoann Duffier ◽  
Audrey Lorthiois ◽  
Pau Cisteró ◽  
Florian Dupuy ◽  
Grégory Jouvion ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Mouse Model ◽  
Humanized Mouse ◽  
Humanized Mouse Model ◽  
In Vivo Evaluation ◽  
Sexual Stages

scholarly journals Anti-CD81 but not anti-SR-BI blocks Plasmodium falciparum liver infection in a humanized mouse model

2015 ◽  
Author(s):  
L. Foquet ◽  
C. C. Hermsen ◽  
L. Verhoye ◽  
G.-J. van Gemert ◽  
R. Cortese ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Mouse Model ◽  
Humanized Mouse ◽  
Humanized Mouse Model ◽  
Liver Infection

scholarly journals Stable Artesunate Resistance in A Humanized Mouse Model of Plasmodium falciparum

2021 ◽  
Author(s):  
Sheetal Saini ◽  
Rajinder Kumar ◽  
Rajeev K. Tyagi
Keyword(s):  
Plasmodium Falciparum ◽  
Combination Therapy ◽  
Malaria Infection ◽  
Artemisinin Resistance ◽  
Antimalarial Drugs ◽  
Humanized Mouse ◽  
Humanized Mouse Model ◽  
Human Malaria

Plasmodium falciparum, the most devastating human malaria parasite, confers higher morbidity and mortality. Although efforts have been made to develop an effective malaria vaccine, stage- and species-specific short-lived immunity crippled these efforts. Hence, antimalarial drug treatment becomes a mainstay for the treatment of malaria infection in the wake of the unavailability of an effective vaccine. Further, there has been a wide array of antimalarial drugs effective against various developmental stages of P. falciparum due to their different structures, modes of action, and pharmacodynamics as well as pharmacokinetics. The development of resistance against almost all frontline drugs by P. falciparum indicates the need for combination therapy (artemisinin-based combination therapy; ACT) to treat patients with P. falciparum. A higher pool of parasitemia under discontinuous in vivo artemisinin drug pressure in a developed humanized mouse allows the selection of artesunate resistant (ART-R) P. falciparum. Intravenously administered artesunate, using either single flash doses or a 2-day regimen, to the P. falciparum-infected human blood chimeric NOD/SCID.IL-2Rγ−/− immunocompromised (NSG) mice, with progressive dose increments upon parasite recovery, was the strategy deployed to select resistant parasites. Parasite susceptibility to artemisinins and other antimalarial compounds was characterized in vitro and in vivo. P. falciparum has shown to evolve extreme artemisinin resistance as well as co-resistance to antimalarial drugs. Overall, the present information shall be very useful in devising newer therapeutic strategies to treat human malaria infection.

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).

Platelet Hypersensitivity in Acute Malaria (Plasmodium falciparum) Infection in Man

1981 ◽  
Vol 46 (02) ◽  
pp. 547-549 ◽  
Author(s):  
E M Essien ◽  
M I Ebhota
Keyword(s):  
Plasmodium Falciparum ◽  
Malaria Infection ◽  
Light Transmission ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Wave Pattern ◽  
Falciparum Infection ◽  
Secondary Wave ◽  
Control Subjects ◽  
The Mean

SummaryDuring acute malaria infection, platelets in human platelet-rich plasma are hypersensitive to the addition of ADP between 1.0 uM and 5.0 uM, or adrenaline 0.11 uM as aggregating agents. The mean maximum aggregation amplitude (as % of light transmission) obtained from 8 subjects in response to added ADP (1.0 uM), 39.8 ± 27 (1SD), was significantly greater than the value in 6 controls (5.2±6.7 (1SD); t = 3, 51 P <0.005). A similar pattern of response was obtained with higher ADP concentrations (2.4,4.5 or 5.0 uM) in 22 patients and 20 control subjects (89.9±14.9% vs 77.8±16.5% (1SD) t = 2.45, P <0.02). Addition of 4.5 uM ADP to patient PRP usually evoked only a single aggregation wave (fused primary and secondary waves) while the typical primary and secondary wave pattern was usually obtained from controls.Mean plasma B-thromboglobulin (BTG) concentration in 7 patients (208.3 ± 15.6 ng/ml) was significantly higher than the value in 6 control subjects (59.2±15.7 ng/ml; t = 13.44, P <0.002).

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