Journal articles: 'Plasmodium berghei ANKA'

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Gorgette, Olivier, Alexandre Existe, Mariama Idrissa Boubou, Sébastien Bagot, Jean-Louis Guénet, Dominique Mazier, Pierre-André Cazenave, and Sylviane Pied. "Deletion of T Cells Bearing the Vβ8.1 T-Cell Receptor following Mouse Mammary Tumor Virus 7 Integration Confers Resistance to Murine Cerebral Malaria." Infection and Immunity 70, no. 7 (July 2002): 3701–6. http://dx.doi.org/10.1128/iai.70.7.3701-3706.2002.

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ABSTRACT Plasmodium berghei ANKA induces a fatal neurological syndrome known as cerebral malaria (CM) in susceptible mice. Host genetic elements are among the key factors determining susceptibility or resistance to CM. Analysis of mice of the same H-2 haplotype revealed that mouse mammary tumor virus 7 (MTV-7) integration into chromosome 1 is one of the key factors associated with resistance to neurological disease during P. berghei ANKA infection. We investigated this phenomenon by infecting a series of recombinant inbred mice (CXD2), derived from BALB/c (susceptible to CM) and DBA/2 (resistant to CM) mice, with P. berghei ANKA. We observed differences in susceptibility to CM induced by this Plasmodium strain. Mice with the MTV-7 sequence in their genome were resistant to CM, whereas those without integration of this gene were susceptible. Thus, an integrated proviral open reading frame or similar genomic sequences may confer protection against neuropathogenesis during malaria, at least in mice.

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Mitchell, Andrew J., Anna M. Hansen, Leia Hee, Helen J. Ball, Sarah M. Potter, John C. Walker, and Nicholas H. Hunt. "Early Cytokine Production Is Associated with Protection from Murine Cerebral Malaria." Infection and Immunity 73, no. 9 (September 2005): 5645–53. http://dx.doi.org/10.1128/iai.73.9.5645-5653.2005.

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ABSTRACT Cerebral malaria (CM) is an infrequent but serious complication of Plasmodium falciparum infection in humans. Animal and human studies suggest that the pathogenesis of CM is immune mediated, but the precise mechanisms leading to cerebral pathology are unclear. In mice, infection with Plasmodium berghei ANKA results in CM on day 6 postinoculation (p.i.), while infection with the closely related strain P. berghei K173 does not result in CM. Infection with P. berghei K173 was associated with increased plasma gamma interferon (IFN-γ) at 24 h p.i. and with increased splenic and hepatic mRNAs for a range of cytokines (IFN-γ, interleukin-10 [IL-10], and IL-12) as well as the immunoregulatory enzyme indoleamine 2,3-dioxygenase. In contrast, P. berghei ANKA infection was associated with an absence of cytokine production at 24 h p.i. but a surge of IFN-γ production at 3 to 4 days p.i. When mice were coinfected with both ANKA and K173, they produced an early cytokine response, including a burst of IFN-γ at 24 h p.i., in a manner similar to animals infected with P. berghei K173 alone. These coinfected mice failed to develop CM. In addition, in a low-dose P. berghei K173 infection model, protection from CM was associated with early production of IFN-γ. Early IFN-γ production was present in NK-cell-depleted, γδ-cell-depleted, and Jα281−/− (NKT-cell-deficient) mice but absent from β2-microglobulin mice that had been infected with P. berghei K173. Taken together, the results suggest that the absence of a regulatory pathway involving IFN-γ and CD8+ T cells in P. berghei ANKA infection allows the development of cerebral immunopathology.

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Briquet, Sylvie, Nadou Lawson-Hogban, Bertrand Boisson, Miguel P. Soares, Roger Péronet, Leanna Smith, Robert Ménard, Michel Huerre, Salah Mécheri, and Catherine Vaquero. "Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity." Infection and Immunity 83, no. 7 (April 27, 2015): 2771–84. http://dx.doi.org/10.1128/iai.03129-14.

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Eukaryotic high-mobility-group-box (HMGB) proteins are nuclear factors involved in chromatin remodeling and transcription regulation. When released into the extracellular milieu, HMGB1 acts as a proinflammatory cytokine that plays a central role in the pathogenesis of several immune-mediated inflammatory diseases. We found that thePlasmodiumgenome encodes two genuine HMGB factors,PlasmodiumHMGB1 and HMGB2, that encompass, like their human counterparts, a proinflammatory domain. Given that these proteins are released from parasitized red blood cells, we then hypothesized thatPlasmodiumHMGB might contribute to the pathogenesis of experimental cerebral malaria (ECM), a lethal neuroinflammatory syndrome that develops in C57BL/6 (susceptible) mice infected withPlasmodium bergheiANKA and that in many aspects resembles human cerebral malaria elicited byP. falciparuminfection. The pathogenesis of experimental cerebral malaria was suppressed in C57BL/6 mice infected withP. bergheiANKA lacking thehmgb2gene (Δhmgb2ANKA), an effect associated with a reduction of histological brain lesions and with lower expression levels of several proinflammatory genes. The incidence of ECM inpbhmgb2-deficient mice was restored by the administration of recombinantPbHMGB2. Protection from experimental cerebral malaria in Δhmgb2ANKA-infected mice was associated with reduced sequestration in the brain of CD4+and CD8+T cells, including CD8+granzyme B+and CD8+IFN-γ+cells, and, to some extent, neutrophils. This was consistent with a reduced parasite sequestration in the brain, lungs, and spleen, though to a lesser extent than in wild-typeP. bergheiANKA-infected mice. In summary,PlasmodiumHMGB2 acts as an alarmin that contributes to the pathogenesis of cerebral malaria.

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Clark, I. A., S. Ilschner, J. D. MacMicking, and W. B. Cowden. "TNF and Plasmodium berghei ANKA-induced cerebral malaria." Immunology Letters 25, no. 1-3 (August 1990): 195–98. http://dx.doi.org/10.1016/0165-2478(90)90114-6.

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Potter, S. M., A. J. Mitchell, W. B. Cowden, L. A. Sanni, M. Dinauer, J. B. de Haan, and N. H. Hunt. "Phagocyte-Derived Reactive Oxygen Species Do Not Influence the Progression of Murine Blood-Stage Malaria Infections." Infection and Immunity 73, no. 8 (August 2005): 4941–47. http://dx.doi.org/10.1128/iai.73.8.4941-4947.2005.

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ABSTRACT Phagocyte-derived reactive oxygen species have been implicated in the clearance of malaria infections. We investigated the progression of five different strains of murine malaria in gp91phox−/− mice, which lack a functional NADPH oxidase and thus the ability to produce phagocyte-derived reactive oxygen species. We found that the absence of functional NADPH oxidase in the gene knockout mice had no effect on the parasitemia or total parasite burden in mice infected with either resolving (Plasmodium yoelii and Plasmodium chabaudi K562) or fatal (Plasmodium berghei ANKA, Plasmodium berghei K173 and Plasmodium vinckei vinckei) strains of malaria. This lack of effect was apparent in both primary and secondary infections with P. yoelii and P. chabaudi. There was also no difference in the presentation of clinical or pathological signs between the gp91phox−/− or wild-type strains of mice infected with malaria. Progression of P. berghei ANKA and P. berghei K173 infections was unchanged in glutathione peroxidase-1 gene knockout mice compared to their wild-type counterparts. The rates of parasitemia progression in gp91phox−/− mice and wild-type mice were not significantly different when they were treated with l-N G -methylarginine, an inhibitor of nitric oxide synthase. These results suggest that phagocyte-derived reactive oxygen species are not crucial for the clearance of malaria parasites, at least in murine models.

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AVISHA, AZARINE NEIRA, and PRAWESTY DIAH UTAMI. "Pengaruh Pemberian Ekstrak Rimpang Temulawak (Curcuma xanthorrhiza Roxb.) Terhadap Jumlah Eritrosit Mencit (Mus musculus L.) Jantan BALB/c yang Diinokulasi Plasmodium Berghei Anka." Hang Tuah Medical journal 15, no. 2 (June 6, 2018): 192. http://dx.doi.org/10.30649/htmj.v15i2.71.

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Malaria masih menjadi salah satu penyakit infeksi yang paling penting di negara tropis karena dapat menyebabkan anemia berat dan kematian. Dewasa ini, penatalaksanaan untuk malaria sendiri semakin terbatas karena adanya resistensi<a href="#_msocom_1">[O11]</a> . Oleh sebab itu, diperlukan adanya penemuan senyawa baru untuk menanggulanginya. Tujuan dari penelitian ini adalah untuk mengetahui pengaruh ekstrak rimpang temulawak (Curcuma xanthorrhiza Roxb.) terhadap jumlah eritrosit mencit (Mus musculus L.) jantan BALB/c yang diinokulasi Plasmodium berghei ANKA. Penelitian dilakukan secara eksperimental dengan desain post-test only control group dengan menggunakan lima kelompok mencit. Satu kelompok mencit dibiarkan normal sedangkan empat kelompok lain diinokulasi Plasmodium berghei ANKA, dimana satu kelompok diberi aquades dan tiga kelompok diterapi ekstrak temulawak (Curcuma xanthorrhiza Roxb.) dengan dosis 150 mg/KgBB, 100 mg/KgBB, dan 50 mg/KgBB selama empat hari. Pada hari kelima dilakukan pemeriksaan darah untuk mengetahui jumlah eritrosit. Hasil penelitian ini menunjukkan bahwa rerata jumlah eritrosit mencit (Mus musculus L.) jantan BALB/c yang diinokulasi Plasmodium berghei ANKA dandiberi ekstrak rimpang temulawak (Curcuma xanthorrhiza Roxb.)dengan dosis 150 mg/KgBB dan 50 mg/KgBB menurun secara tidak bermakna. Sedangkan rerata jumlah eritrosit mencit (Mus musculus L.) jantan BALB/c yang diinokulasi Plasmodium berghei ANKA dan diberi ekstrak rimpang temulawak (Curcuma xanthorrhiza Roxb.) dengan dosis 100 mg/KgBB menurun bermakna (p=0,004). Kata Kunci: Malaria, temulawak (Curcuma xanthorrhiza Roxb.), Eritrosit, Plasmodium berghei ANKA.<div><hr align="left" size="1" width="33%" /><div><div> <a href="#_msoanchor_1">[O11]</a>Resistensi terhadap apa?</div></div></div>

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Haddad, Diana, Jorge Maciel, and Nirbhay Kumar. "Infection with Plasmodium berghei Boosts Antibody Responses Primed by a DNA Vaccine Encoding Gametocyte Antigen Pbs48/45." Infection and Immunity 74, no. 4 (April 2006): 2043–51. http://dx.doi.org/10.1128/iai.74.4.2043-2051.2006.

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ABSTRACT An important consideration in the development of a malaria vaccine for individuals living in areas of endemicity is whether vaccine-elicited immune responses can be boosted by natural infection. To investigate this question, we used Plasmodium berghei ANKA blood-stage parasites for the infection of mice that were previously immunized with a DNA vaccine encoding the P. berghei sexual-stage antigen Pbs48/45. Intramuscular immunization in mice with one or two doses of DNA-Pbs48/45 or of empty DNA vaccine as control did not elicit detectable anti-Pbs48/45 antibodies as determined by enzyme-linked immunosorbent assay. An infection with P. berghei ANKA 6 weeks after DNA vaccination elicited comparable anti-Pbs48/45 antibody levels in mice which had been primed with DNA-Pbs48/45 or with empty DNA vaccine. However, a repeat infection with P. berghei ANKA resulted in significantly higher anti-Pbs48/45 antibody levels in mice which had been primed with the DNA-Pbs48/45 vaccine than the levels in the mock DNA-vaccinated mice. In parallel and as an additional control to distinguish the boosting of Pbs48/45 antibodies exclusively by gametocytes during infection, a separate group of mice primed with DNA-Pbs48/45 received an infection with P. berghei ANKA clone 2.33, which was previously described as a “nongametocyte producer.” To our surprise, this parasite clone too elicited antibody levels comparable to those induced by the P. berghei gametocyte producer clone. We further demonstrate that the nongametocyte producer P. berghei clone is in fact a defective gametocyte producer that expresses Pbs48/45, much like the gametocyte producer clone, and is therefore capable of boosting antibody levels to Pbs48/45. Taken together, these results indicate that vaccine-primed antibodies can be boosted during repeat infections and warrant further investigation with additional malaria antigens.

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Ndung'u, Loise, Benard Langat, Esther Magiri, Joseph Ng'ang'a, Beatrice Irungu, Alexis Nzila, and Daniel Kiboi. "Amodiaquine resistance in Plasmodium berghei is associated with PbCRT His95Pro mutation, loss of chloroquine, artemisinin and primaquine sensitivity, and high transcript levels of key transporters." Wellcome Open Research 2 (June 20, 2017): 44. http://dx.doi.org/10.12688/wellcomeopenres.11768.1.

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Background: The human malaria parasite Plasmodium falciparum has evolved complex drug evasion mechanisms to all available antimalarials. To date, the combination of amodiaquine-artesunate is among the drug of choice for treatment of uncomplicated malaria. In this combination, a short acting, artesunate is partnered with long acting, amodiaquine for which resistance may emerge rapidly especially in high transmission settings. Here, we used a rodent malaria parasite Plasmodium berghei ANKA as a surrogate of P. falciparum to investigate the mechanisms of amodiaquine resistance. Methods: We used serial technique to select amodiaquine resistance by submitting the parasites to continuous amodiaquine pressure. We then employed the 4-Day Suppressive Test to monitor emergence of resistance and determine the cross-resistance profiles. Finally, we genotyped the resistant parasite by PCR amplification, sequencing and relative quantitation of mRNA transcript of targeted genes. Results: Submission of P. berghei ANKA to amodiaquine pressure yielded resistant parasite within thirty-six passages. The effective dosage that reduced 90% of parasitaemia (ED90) of sensitive line and resistant line were 4.29mg/kg and 19.13mg/kg, respectively. After freezing at -80ºC for one month, the resistant parasite remained stable with an ED90 of 18.22mg/kg. Amodiaquine resistant parasites are also resistant to chloroquine (6fold), artemether (10fold), primaquine (5fold), piperaquine (2fold) and lumefantrine (3fold). Sequence analysis of Plasmodium berghei chloroquine resistant transporter revealed His95Pro mutation. No variation was identified in Plasmodium berghei multidrug resistance gene-1 (Pbmdr1), Plasmodium berghei deubiquitinating enzyme-1 or Plasmodium berghei Kelch13 domain nucleotide sequences. Amodiaquine resistance is also accompanied by high mRNA transcripts of key transporters; Pbmdr1, V-type/H+ pumping pyrophosphatase-2 and sodium hydrogen ion exchanger-1 and Ca2+/H+ antiporter. Conclusions: Selection of amodiaquine resistance yielded stable “multidrug-resistant’’ parasites and thus may be used to study common resistance mechanisms associated with other antimalarial drugs. Genome wide studies may elucidate other functionally important genes controlling AQ resistance in P. berghei.

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Gumede, Bonginkosi, Peter Folb, and Bernhard Ryffel. "Oral artesunate prevents Plasmodium berghei Anka infection in mice." Parasitology International 52, no. 1 (March 2003): 53–59. http://dx.doi.org/10.1016/s1383-5769(02)00081-8.

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HERMSEN, C., T. VAN DE WIEL, E. MOMMERS, R. SAUERWEIN, and W. ELING. "Depletion of CD4+ or CD8+ T-cells prevents Plasmodium berghei induced cerebral malaria in end-stage disease." Parasitology 114, no. 1 (January 1997): 7–12. http://dx.doi.org/10.1017/s0031182096008293.

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The role of T-cells in development of experimental cerebral malaria was analysed in C57B1/6J and C57B1/10 mice infected with Plasmodium berghei K173 or Plasmodium berghei ANKA by treatment with anti-CD4 or anti-CD8 mAbs. Mice were protected against cerebral malaria (CM) when anti-CD4 or anti-CD8 mAbs were injected before or during infection. Even in mice in end-stage disease, i.e. with a body temperature below 35·5 °C, treatment with anti-CD4 or anti-CD8 antibodies or the combination protected against CM, whereas chloroquine treatment was completely ineffective in inhibiting further development of the cerebral syndrome.

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Amani, Véronique, Mariama Idrissa Boubou, Sylviane Pied, Myriam Marussig, David Walliker, Dominique Mazier, and Laurent Rénia. "Cloned Lines of Plasmodium berghei ANKA Differ in Their Abilities To Induce Experimental Cerebral Malaria." Infection and Immunity 66, no. 9 (September 1, 1998): 4093–99. http://dx.doi.org/10.1128/iai.66.9.4093-4099.1998.

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ABSTRACT Infection with Plasmodium berghei ANKA is usually lethal. The parasite causes in some mouse strains a neurovascular syndrome, experimental cerebral malaria (ECM), involving immunopathological reactions. The effects on the development of ECM of the mouse genetic background have been clearly demonstrated, but nothing is known about the effects of the clonal diversity of the parasite. We showed that various cloned lines derived from a polyclonal line of P. berghei ANKA caused ECM but that the extent of ECM induction was dependent on the amount of inoculum. Subtle differences in ECM characteristics (survival time and hypothermia) were also observed. We also confirmed, using the 1.49L cloned line, that the mouse genetic background strongly affects ECM.

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DING, YAN, WENYUE XU, TAOLI ZHOU, TAIPING LIU, HONG ZHENG, and YONG FU. "Establishment of a murine model of cerebral malaria in KunMing mice infected with Plasmodium berghei ANKA." Parasitology 143, no. 12 (August 24, 2016): 1672–80. http://dx.doi.org/10.1017/s0031182016001475.

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SUMMARYMalaria remains one of the most devastating diseases. Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection resulting in high mortality and morbidity worldwide. Analysis of precise mechanisms of CM in humans is difficult for ethical reasons and animal models of CM have been employed to study malaria pathogenesis. Here, we describe a new experimental cerebral malaria (ECM) model with Plasmodium berghei ANKA infection in KunMing (KM) mice. KM mice developed ECM after blood-stage or sporozoites infection, and the development of ECM in KM mice has a dose-dependent relationship with sporozoites inoculums. Histopathological findings revealed important features associated with ECM, including accumulation of mononuclear cells and red blood cells in brain microvascular, and brain parenchymal haemorrhages. Blood–brain barrier (BBB) examination showed that BBB disruption was present in infected KM mice when displaying clinical signs of CM. In vivo bioluminescent imaging experiment indicated that parasitized red blood cells accumulated in most vital organs including heart, lung, spleen, kidney, liver and brain. The levels of inflammatory cytokines interferon-gamma, tumour necrosis factor-alpha, interleukin (IL)-17, IL-12, IL-6 and IL-10 were all remarkably increased in KM mice infected with P. berghei ANKA. This study indicates that P. berghei ANKA infection in KM mice can be used as ECM model to extend further research on genetic, pharmacological and vaccine studies of CM.

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Yañez, D. M., J. Batchelder, H. C. van der Heyde, D. D. Manning, and W. P. Weidanz. "γδ T-Cell Function in Pathogenesis of Cerebral Malaria in Mice Infected with Plasmodium bergheiANKA." Infection and Immunity 67, no. 1 (January 1, 1999): 446–48. http://dx.doi.org/10.1128/iai.67.1.446-448.1999.

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ABSTRACT Mice depleted of γδ T cells by monoclonal antibody treatment and infected with Plasmodium berghei ANKA did not develop cerebral malaria (CM). In striking contrast, δ0/0 mice infected with P. berghei developed CM despite their γδ T-cell deficiency. γδ T cells appear to be essential for the pathogenesis of CM in mice having experienced normal ontogeny but not in mice genetically deprived of γδ T cells from the beginning of life.

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Kimani, S. K., J. K. Nganga, D. W. Kariuki, J. Kinyua, F. T. Kimani, and D. M. Kiboi. "Plasmodium berghei ANKA: Selection of pyronaridine resistance in mouse model." African Journal of Biochemistry Research 8, no. 6 (August 15, 2014): 111–17. http://dx.doi.org/10.5897/ajbr2014.0780.

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Utami, Prawesty Diah, and Herin Setianingsih. "Protection of Renal Function ByHyperbaric OxygenDuring Plasmodium berghei ANKA Infection." International Journal of ChemTech Research 13, no. 1 (2020): 69–74. http://dx.doi.org/10.20902/ijctr.2019.130108.

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Background:Malaria cases have consistently increased and the number of deaths remains largely unchanged.Malaria associated renal injury has a high level of morbidity and mortality. High level of blood urea nitrogen / BUN and plasma creatinine is one of the major factors associated with mortality in humans infected with malaria, indicating that impairment of renal function. HBO is widely used as an adjunctive therapy for many diseases, it is known that HBO hasan action as antiplasmodium, antiinflammation and antioxidant effects. Objective: The aim of this study was to determine the effect of HBO on BUN and creatinine levels in rats infected with P. berghei ANKA. Methods:This research was conducted experimentally post-test only control group on six groups of rats. The samples used were 24 male Rattus norvegicus wistar strain that have been infected by Plasmodium bergheiANKA and divided into 6 groups. Group 1 was given combination artesunate and 1, 5 ATA HBO, grup 2 was given combination artesunate and 3, 0 ATA HBO, group 3 was given 1, 5 ATA HBO, group 4 was given 3, 0 ATA HBO, group 5 was given artesunate and group 6 was given aquadest. HBO therapy is carried out for 10 days and the observation of the levels of BUN and creatinine in mice after treatment on tenth day. Results:Descriptive analysis and statistical analysis (Kruskal wallis snd Mann whitney U posthoc) showed a significant difference (p < α = 0.05) on mean levels of BUN and creatinine group receiving combination of artesunate and HBO 3,0 ATA compared to other groups.Hyperbaric oxygen has the effect of reducing the levels of BUN and creatinine in rats infected by P.berghei ANKA.

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Fonager, Jannik, Erica M. Pasini, Joanna A. M. Braks, Onny Klop, Jai Ramesar, Edmond J. Remarque, Irene O. C. M. Vroegrijk, et al. "Reduced CD36-dependent tissue sequestration of Plasmodium-infected erythrocytes is detrimental to malaria parasite growth in vivo." Journal of Experimental Medicine 209, no. 1 (December 19, 2011): 93–107. http://dx.doi.org/10.1084/jem.20110762.

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Adherence of parasite-infected red blood cells (irbc) to the vascular endothelium of organs plays a key role in the pathogenesis of Plasmodium falciparum malaria. The prevailing hypothesis of why irbc adhere and sequester in tissues is that this acts as a mechanism of avoiding spleen-mediated clearance. Irbc of the rodent parasite Plasmodium berghei ANKA sequester in a fashion analogous to P. falciparum by adhering to the host receptor CD36. To experimentally determine the significance of sequestration for parasite growth, we generated a mutant P. berghei ANKA parasite with a reduced CD36-mediated adherence. Although the cognate parasite ligand binding to CD36 is unknown, we show that nonsequestering parasites have reduced growth and we provide evidence that in addition to avoiding spleen removal, other factors related to CD36-mediated sequestration are beneficial for parasite growth. These results reveal for the first time the importance of sequestration to a malaria infection, with implications for the development of strategies aimed at reducing pathology by inhibiting tissue sequestration.

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Clark, Catherine J., Gillian M. Mackay, George A. Smythe, Sonia Bustamante, Trevor W. Stone, and R. Stephen Phillips. "Prolonged Survival of a Murine Model of Cerebral Malaria by Kynurenine Pathway Inhibition." Infection and Immunity 73, no. 8 (August 2005): 5249–51. http://dx.doi.org/10.1128/iai.73.8.5249-5251.2005.

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ABSTRACT C57BL/6J mice infected with Plasmodium berghei ANKA develop neurological dysfunction and die within 7 days of infection. We show that treatment of infected mice with a kynurenine-3-hydroxylase inhibitor prevents them from developing neurological symptoms and extends their life span threefold until severe anemia develops.

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Ribot, Julie C., Rita Neres, Vanessa Zuzarte-Luís, Anita Q. Gomes, Liliana Mancio-Silva, Sofia Mensurado, Daniel Pinto-Neves, et al. "γδ-T cells promote IFN-γ–dependent Plasmodium pathogenesis upon liver-stage infection." Proceedings of the National Academy of Sciences 116, no. 20 (April 26, 2019): 9979–88. http://dx.doi.org/10.1073/pnas.1814440116.

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Cerebral malaria (CM) is a major cause of death due to Plasmodium infection. Both parasite and host factors contribute to the onset of CM, but the precise cellular and molecular mechanisms that contribute to its pathogenesis remain poorly characterized. Unlike conventional αβ-T cells, previous studies on murine γδ-T cells failed to identify a nonredundant role for this T cell subset in experimental cerebral malaria (ECM). Here we show that mice lacking γδ-T cells are resistant to ECM when infected with Plasmodium berghei ANKA sporozoites, the liver-infective form of the parasite and the natural route of infection, in contrast with their susceptible phenotype if challenged with P. berghei ANKA-infected red blood cells that bypass the liver stage of infection. Strikingly, the presence of γδ-T cells enhanced the expression of Plasmodium immunogenic factors and exacerbated subsequent systemic and brain-infiltrating inflammatory αβ-T cell responses. These phenomena were dependent on the proinflammatory cytokine IFN-γ, which was required during liver stage for modulation of the parasite transcriptome, as well as for downstream immune-mediated pathology. Our work reveals an unanticipated critical role of γδ-T cells in the development of ECM upon Plasmodium liver-stage infection.

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Dogruman-Al, Funda, Ayşe Başak Engin, Neslihan Bukan, Seda Evirgen-Bostanci, and Kemal Çeber. "Late-stage systemic immune effectors in Plasmodium berghei ANKA infection: biopterin and oxidative stress." Pteridines 26, no. 3 (September 1, 2015): 105–12. http://dx.doi.org/10.1515/pterid-2014-0019.

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AbstractTo investigate the involvement of systemic oxidative stress in the pathogenesis of murine cerebral malaria, mice were infected with the Plasmodium berghei (P. berghei) ANKA 6653 strain. Serum tryptophan (Trp), kynurenine and urinary biopterin, liver, brain, spleen and serum superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA) and nitrite and nitrate (NOx) levels were measured on day 7 post-inoculation. Our data showed a significant decrease in SOD and an increase in GPx activity and MDA level in all the examined biological materials (p<0.05), except spleen. Conversely, GPx activities in spleen were depleted, while SOD and MDA levels remained unchanged. Increased MDA levels might indicate increased peroxynitrite production, lipid peroxidation and oxidative stress. Also, elevated urinary biopterin, which was accompanied by increased NOx (p<0.05), may support the inhibition of Trp degradation (p>0.05). The excessive NO synthesis in P. berghei infection may be related to the up-regulation of inducible NO synthase, which was in accordance with the increased biopterin excretion. Thus, the large quantities of released toxic redox active radicals attack cell membranes and induce lipid peroxidation. Although P. berghei infection did not demonstrate systemic Trp degradation and related indoleamine-2,3-dioxygenase activity, it may cause multi-organ failure and death, owing to host-derived severe oxidative stress.

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Ekasari, Wiwied, Nindya Tresiana, Suciati Iryani, Tutik Sri Wahyuni, and Heny Arwaty. "Aktivitas Penghambatan Ekstrak Etanol Daun Cassia Spectabilis Terhadap Pertumbuhan Plasmodium falciparum dan Plasmodium berghei." JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA 3, no. 1 (August 4, 2017): 17. http://dx.doi.org/10.20473/jfiki.v3i1.4088.

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Background: Antimalarial screening against nine species of the genus Cassia showed that the methanol extract of leaves Cassia spectabilis have the highest activity. Since it will be used as a traditional medicine, hence it is needed further studies of antimalarial activity of these plants by choosing a safer solvent, namely ethanol. Objective: In vitro anti-malarial activity against Plasmodium falciparum was conducted using the method of Trager and Jensen. Methods: The serial solution tested were: 100, 10, 1, 0.1 and 0.01 µg/ mL, while the in vivo test was performed based on Peter’s test (The days suppressive test) that using P. berghei (strain ANKA) infected mice. Results: The results showed that ethanolic extract of C. spectabilis leaves has inhibitory activity against P. falciparum with IC50 value of 12.52 µg/ mL and against P. berghei with ED50 value of 131.5 mg/kg body weight. Conclusions: A further study to see the potential of ethanol extract from C. Spectabilis leaves as anti-malaria is warranted.

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Ekasari, Wiwied, Nindya Tresiana, Suciati Iryani, Tutik Sri Wahyuni, and Heny Arwaty. "Aktivitas Penghambatan Ekstrak Etanol Daun Cassia Spectabilis Terhadap Pertumbuhan Plasmodium falciparum dan Plasmodium berghei." JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA 3, no. 1 (August 4, 2017): 17. http://dx.doi.org/10.20473/jfiki.v3i12016.17-21.

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Background: Antimalarial screening against nine species of the genus Cassia showed that the methanol extract of leaves Cassia spectabilis have the highest activity. Since it will be used as a traditional medicine, hence it is needed further studies of antimalarial activity of these plants by choosing a safer solvent, namely ethanol. Objective: In vitro anti-malarial activity against Plasmodium falciparum was conducted using the method of Trager and Jensen. Methods: The serial solution tested were: 100, 10, 1, 0.1 and 0.01 µg/ mL, while the in vivo test was performed based on Peter’s test (The days suppressive test) that using P. berghei (strain ANKA) infected mice. Results: The results showed that ethanolic extract of C. spectabilis leaves has inhibitory activity against P. falciparum with IC50 value of 12.52 µg/ mL and against P. berghei with ED50 value of 131.5 mg/kg body weight. Conclusions: A further study to see the potential of ethanol extract from C. Spectabilis leaves as anti-malaria is warranted.

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Keswani, Tarun, Anirban Sengupta, Samrat Sarkar, and Arindam Bhattacharyya. "Dendritic cells subsets mediated immune response during Plasmodium berghei ANKA and Plasmodium yoelii infection." Cytokine 73, no. 2 (June 2015): 198–206. http://dx.doi.org/10.1016/j.cyto.2015.02.023.

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Kwon, Sangwoo, Dong‐Hun Lee, Se‐Jik Han, Woochul Yang, Fu‐Shi Quan, and Kyung Sook Kim. "Biomechanical properties of red blood cells infected by Plasmodium berghei ANKA." Journal of Cellular Physiology 234, no. 11 (April 15, 2019): 20546–53. http://dx.doi.org/10.1002/jcp.28654.

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Pan, Yanyan, Xiaodan Sun, Danni Li, Yan Zhao, Feng Jin, and Yaming Cao. "PD-1 blockade promotes immune memory following Plasmodium berghei ANKA reinfection." International Immunopharmacology 80 (March 2020): 106186. http://dx.doi.org/10.1016/j.intimp.2020.106186.

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ARSYA, MUHAMMAD REYHAN, PRAWESTY DIAH UTAMI, and IRMAWATI IRMAWATI. "Pengaruh Pemberian Ekstrak Temulawak (Curcuma Xanthorrizha Roxb.) Terhadap Level Nekrosis pada Jaringan Lien Mencit Putih (Mus Musculus L.) Jantan Galur Balb/C yang Diinokulasi Plasmodium berghei anka." Hang Tuah Medical journal 16, no. 2 (June 13, 2019): 186. http://dx.doi.org/10.30649/htmj.v16i2.122.

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AbstractBackground : Malaria is a disease caused by the Plasmodium parasite and is transmitted by the Anopheles mosquito and is still a health problem in Indonesia due to high mortality and morbidity. One form of a severe complication of malaria in addition to cerebral malaria is a function failure of the spleen. Today, the management of malaria is increasingly limited due to resistance. Therefore, further development is needed to find new innovations in malaria treatment.Purpose : The purpose of this study was to determine the effect of temulawak rhizome extract (Curcuma xanthorhizza Roxb.) On the level of necrosis in the spleen tissue of male BALB / c mice (Mus musculus L.) inoculated with Plasmodium berghei ANKA.Methods :Experimental research used a post-test only control group design that used five groups of mice. One group of mice was left normal while the other four groups were inoculated with Plasmodium berghei ANKA, positive control groups were given aquades and three treatment groups treated with temulawak extract (Curcuma xanthorrhiza Roxb.) With a dose of 150 mg / KgBB, 100 mg / KgBB, and 50 mg / KgBB for four day. On the fifth day an observation of the level of necrosis in the spleen organ of mice to determine the level of necrosis by histopathological examination using a light microscope.Conclusion and Result : The results of this study indicate that the administration of ginger rhizome extract (Curcuma xanthorriza Roxb.) Has an influence on the level of necrosis of male mice (Mus musculus L.) BALB / c inoculated with Plasmodium berghei ANKA α = 0,002 (ρ<0,05), where the administration of temulawak extract can increase necrosis levels compared to the control group . This is probably due to the lack of temulawak extract dosage and lack of observation in this study. Keywords : Malaria, curcuma (Curcuma xanthorrhiza Roxb.), Necrosis level, Plasmodium berghei ANKA

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Belnoue, Elodie, Fabio T. M. Costa, Ana M. Vigário, Tatiana Voza, Françoise Gonnet, Irène Landau, Nico van Rooijen, Matthias Mack, William A. Kuziel, and Laurent Rénia. "Chemokine Receptor CCR2 Is Not Essential for the Development of Experimental Cerebral Malaria." Infection and Immunity 71, no. 6 (June 2003): 3648–51. http://dx.doi.org/10.1128/iai.71.6.3648-3651.2003.

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ABSTRACT Infection with Plasmodium berghei ANKA induces cerebral malaria in susceptible mice. Brain-sequestered CD8+ T cells are responsible for this pathology. We have evaluated the role of CCR2, a chemokine receptor expressed on CD8+ T cells. Infected CCR2-deficient mice were as susceptible to cerebral malaria as wild-type mice were, and CD8+ T-cell migration to the brain was not abolished.

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Aini, Kholida Nur, Windya Tri Hapsari, Kartika Arum Wardani, Heny Arwati, and Willy Sandhika. "Antimalarial activity of goat bile against Plasmodium berghei ANKA infection in BALB/c mice." Qanun Medika - Medical Journal Faculty of Medicine Muhammadiyah Surabaya 4, no. 2 (July 29, 2020): 187. http://dx.doi.org/10.30651/jqm.v4i2.3540.

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Abstract Goat bile has been used by some Indonesian people to treat malaria and increase their stamina. This study aimed to prove whether goat bile toxic or not in BALB/c mice and to verify the antimalarial activity of goat bile at various concentrations in mice infected with Plasmodium berghei ANKA. Acute toxicity test was performed using twenty male BALB/c mice with an average body weight of 25 grams, which were divided into four groups. Mice were given 25%, 50%, and 100% goat bile, respectively, while negative control was given distilled water. Any change in weight, odor, color, agitation, appearance, color of urine and feces, coma, and death, were recorded. A different set of mice were infected with P. berghei ANKA. This study conducted using the posttest only control group design with four treatments and five replications. A four day-treatment of goat bile was given by oral gavage to find out its effect on parasitemia level. Infected mice were divided randomly into 4 groups, where the GBNeg group as negative control was given only distilled water. The GB25, GB50, and GB100 groups were treated with 25%, 50%, and 100% goat bile, respectively. The parasitemia was observed daily on Giemsa-stained tail blood smears of each mice. No death or other sign of toxicity was found in goat bile-treated mice. Goat bile showed anti-malarial activity. The parasitemia in all goat bile treated groups was lower compared with the negative control group. The ED50 of goat bile against the growth of parasite was 48,55 %. Goat bile is a potential source of new antimalarial therapies. Further investigations are recommended to yield new anti-malarial drug candidates. Keywords : Goat bile, parasitemia, Plasmodium berghei ANKA, ED50Correspondence : heny-a@fk.unair.ac.id

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Nie, Catherine Q., Nicholas J. Bernard, Louis Schofield, and Diana S. Hansen. "CD4+ CD25+ Regulatory T Cells Suppress CD4+ T-Cell Function and Inhibit the Development of Plasmodium berghei-Specific TH1 Responses Involved in Cerebral Malaria Pathogenesis." Infection and Immunity 75, no. 5 (February 26, 2007): 2275–82. http://dx.doi.org/10.1128/iai.01783-06.

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ABSTRACT The infection of mice with Plasmodium berghei ANKA constitutes the best available mouse model for human Plasmodium falciparum-mediated cerebral malaria, a devastating neurological syndrome that kills nearly 2.5 million people every year. Experimental data suggest that cerebral disease results from the sequestration of parasitized erythrocytes within brain blood vessels, which is exacerbated by host proinflammatory responses mediated by cytokines and effector cells including T lymphocytes. Here, T cell responses to P. berghei ANKA were analyzed in cerebral malaria-resistant and -susceptible mouse strains. CD4+ T-cell proliferation and interleukin-2 (IL-2) production in response to parasite-specific and polyclonal stimuli were strongly inhibited in cerebral malaria-resistant mice. In vitro and in vivo depletion of CD4+ CD25+ regulatory T (Treg) cells significantly reversed the inhibition of CD4+ T-cell proliferation and IL-2 production, indicating that this cell population contributes to the suppression of T-cell function during malaria. Moreover, in vivo depletion of Treg cells prevented the development of parasite-specific TH1 cells involved in the induction of cerebral malaria during a secondary parasitic challenge, demonstrating a regulatory role for this cell population in the control of pathogenic responses leading to fatal disease.

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Ndung'u, Loise, Benard Langat, Esther Magiri, Joseph Ng'ang'a, Beatrice Irungu, Alexis Nzila, and Daniel Kiboi. "Amodiaquine resistance in Plasmodium berghei is associated with PbCRT His95Pro mutation, loss of chloroquine, artemisinin and primaquine sensitivity, and high transcript levels of key transporters." Wellcome Open Research 2 (June 6, 2018): 44. http://dx.doi.org/10.12688/wellcomeopenres.11768.2.

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Background: The human malaria parasite Plasmodium falciparum has evolved drug evasion mechanisms to all available antimalarials. The combination of amodiaquine-artesunate is among the drug of choice for treatment of uncomplicated malaria. In this combination, a short-acting, artesunate is partnered with long-acting, amodiaquine for which resistance may emerge rapidly especially in high transmission settings. Here, we used a rodent malaria parasite Plasmodium berghei ANKA as a surrogate of P. falciparum to investigate the mechanisms of amodiaquine resistance. Methods: We used the ramp up approach to select amodiaquine resistance. We then employed the 4-Day Suppressive Test to measure the resistance level and determine the cross-resistance profiles. Finally, we genotyped the resistant parasite by PCR amplification, sequencing and relative quantitation of mRNA transcript of targeted genes. Results: Submission of the parasite to amodiaquine pressure yielded resistant line within thirty-six passages. The effective doses that reduced 90% of parasitaemia (ED90) of the sensitive and resistant lines were 4.29mg/kg and 19.13mg/kg respectively. The selected parasite retained resistance after ten passage cycles in the absence of the drug and freezing at -80ºC for one month with ED90 of 20.34mg/kg and 18.22mg/kg. The parasite lost susceptibility to chloroquine by (6-fold), artemether (10-fold), primaquine (5-fold), piperaquine (2-fold) and lumefantrine (3-fold). Sequence analysis of Plasmodium berghei chloroquine-resistant transporter revealed His95Pro mutation. We found no variation in the nucleotide sequences of Plasmodium berghei multidrug resistance gene-1 (Pbmdr1), Plasmodium berghei deubiquitinating enzyme-1 or Plasmodium berghei Kelch13 domain. However, high mRNA transcripts of essential transporters; Pbmdr1, V-type/H+ pumping pyrophosphatase-2 and sodium hydrogen ion exchanger-1 and Ca2+/H+ antiporter accompanies amodiaquine resistance. Conclusions: The selection of amodiaquine resistance yielded stable “multidrug-resistant’’ parasites and thus may be used to study shared resistance mechanisms associated with other antimalarial drugs. Genome-wide analysis of the parasite may elucidate other functionally relevant genes controlling AQ resistance in P. berghei.

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Sunita, K., P. V. V. Satish, and DSantha Kumari. "Antiplasmodial efficacy of Calotropis gigantea (L.) against Plasmodium falciparum (3D7 strain) and Plasmodium berghei (ANKA)." Journal of Vector Borne Diseases 54, no. 3 (2017): 215. http://dx.doi.org/10.4103/0972-9062.217612.

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Goschnick, M. W., C. G. Black, L. Kedzierski, A. A. Holder, and R. L. Coppel. "Merozoite Surface Protein 4/5 Provides Protection against Lethal Challenge with a Heterologous Malaria Parasite Strain." Infection and Immunity 72, no. 10 (October 2004): 5840–49. http://dx.doi.org/10.1128/iai.72.10.5840-5849.2004.

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ABSTRACT Immunization with merozoite surface protein 4/5 (MSP4/5), the murine malaria homologue of Plasmodium falciparum MSP4 and MSP5, has been shown to protect mice against challenge by parasites expressing the homologous form of the protein. The gene encoding MSP4/5 was sequenced from a number of Plasmodium yoelii isolates in order to assess the level of polymorphism in the protein. The gene was found to be highly conserved among the 13 P. yoelii isolates sequenced, even though many of the same isolates showed pronounced variability in their MSP119 sequences. Nonsynonymous mutations were detected only for the isolates Plasmodium yoelii nigeriensis N67 and Plasmodium yoelii killicki 193L and 194ZZ. Immunization and challenge of BALB/c mice showed that the heterologous MSP4/5 proteins were able to confer a level of protection against lethal Plasmodium yoelii yoelii YM challenge infection similar to that induced by immunization with the homologous MSP4/5 protein. To explore the limits of heterologous protection, mice were immunized with recombinant MSP4/5 protein from Plasmodium berghei ANKA and Plasmodium chabaudi adami DS and challenged with P. y. yoelii YM. Interestingly, significant protection was afforded by P. berghei ANKA MSP4/5, which shows 81% sequence identity with P. y. yoelii YM MSP4/5, but it was abolished upon reduction and alkylation. Significant protection was not observed for mice immunized with recombinant P. c. adami DS MSP4/5, which shows 55.7% sequence identity with P. y. yoelii YM MSP4/5. This study demonstrates the robustness of MSP4/5 in conferring protection against variant forms of the protein in a murine challenge system, in contrast to the situation found for other asexual-stage proteins, such as MSP119 and AMA1.

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Huang, Bo, Man Liu, Shiguang Huang, Bin Wu, Hong Guo, Xin-zhuan Su, and Fangli Lu. "Expression of Tim-1 and Tim-3 in Plasmodium berghei ANKA infection." Parasitology Research 112, no. 7 (May 8, 2013): 2713–19. http://dx.doi.org/10.1007/s00436-013-3442-z.

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Cervantes-Candelas, Luis Antonio, Jesús Aguilar-Castro, Fidel Orlando Buendía-González, Omar Fernández-Rivera, Armando Cervantes-Sandoval, Jorge Morales-Montor, and Martha Legorreta-Herrera. "Tamoxifen Suppresses the Immune Response to Plasmodium berghei ANKA and Exacerbates Symptomatology." Pathogens 10, no. 6 (June 12, 2021): 743. http://dx.doi.org/10.3390/pathogens10060743.

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Malaria is the most lethal parasitic disease in the world. Mortality and severity in symptoms are higher in men than women, suggesting that oestrogens, which are in higher concentration in females than in males, may regulate the immune response against malaria. Tamoxifen, a selective oestrogen receptor modulator used in breast cancer treatment due to its antagonistic effect on oestrogen receptors α and β, is also studied because of its potential therapeutic use for several parasitic diseases. However, most studies, including one in malaria, have not addressed the immunomodulatory role of tamoxifen. In this work, we evaluated the effect of tamoxifen on the immune response of CBA/Ca mice against Plasmodium berghei ANKA. This study showed for the first time that tamoxifen increased parasite load, aggravated symptoms by decreasing body temperature and body weight, and worsened anaemia. Additionally, tamoxifen significantly increased the splenic index and the percentages of CD4+ and NK+ cells on day eight post-infection. By contrast, tamoxifen decreased both CD8+ and B220+ populations in the spleen and decreased the serum levels of IL-2, IL-6, and IL-17. Our findings support the notion that tamoxifen is a potent immunomodulator in malaria-infected mice and suggest caution when administering it to malaria-infected women with breast cancer.

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Onohuean, Hope, Abdullateef I. Alagbonsi, Ibe M. Usman, Keneth Iceland Kasozi, Athanasios Alexiou, Reem H. Badr, Gaber El-Saber Batiha, and Joseph O. C. Ezeonwumelu. "Annona muricata Linn and Khaya grandifoliola C.DC. Reduce Oxidative Stress In Vitro and Ameliorate Plasmodium berghei-Induced Parasitemia and Cytokines in BALB/c Mice." Journal of Evidence-Based Integrative Medicine 26 (January 1, 2021): 2515690X2110366. http://dx.doi.org/10.1177/2515690x211036669.

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Background. Annona muricata and Khaya grandifoliola are ethnomedicinally used for the treatment of malaria and have been experimentally shown to have an anti-plasmodial effect, but the mechanisms involved are not fully understood. This study investigated the effect of the ethanol extracts of their leaves on parasitemia, radical scavenging and cytokines in Plasmodium berghei ANKA-infected BALB/c mice. Methods. BALB/c mice were infected with P. berghei and treated with chloroquine, A. muricata or K. grandifoliola extract for 4 days. The percentage of parasitemia and the level of cytokine expression were determined after treatment. Trace element, phytochemical and nitric oxide (NO) scavenging activity, 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging properties assays were done to study the antioxidant effects of AN and KG in vitro. Results. P. berghei consistently increased parasitemia in BALB/c mice. The tested doses (100-, 200-, and 400 mg/kg) of A. muricata and K. grandifoliola attenuated the P. berghei-induced elevation of parasitemia and cytokines (TNF-α, IL-5, and IL-6) in vivo during the experimental period, though not as much as chloroquine. Moreover, both extracts scavenged the DPPH and NO radicals, though A. muricata had more anti-oxidant effect than K. grandifoliola in-vitro. Conclusion. The ethanol extracts of A. muricata and K. grandifoliola reduce parasitemia in P. berghei-treated mice BALB/c by scavenging free radicals and reducing cytokines, though the extracts were not as effective as chloroquine.

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Voza, Tatiana, Ana M. Vigário, Elodie Belnoue, Anne Charlotte Grüner, Jean-Christophe Deschemin, Michèle Kayibanda, Florian Delmas, et al. "Species-Specific Inhibition of Cerebral Malaria in Mice Coinfected with Plasmodium spp." Infection and Immunity 73, no. 8 (August 2005): 4777–86. http://dx.doi.org/10.1128/iai.73.8.4777-4786.2005.

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ABSTRACT Recent epidemiological observations suggest that clinical evolution of Plasmodium falciparum infections might be influenced by the concurrent presence of another Plasmodium species, and such mixed-species infections are now known to occur frequently in residents of most areas of endemicity. We used mice infected with P. berghei ANKA (PbA), a model for cerebral malaria (CM), to investigate the influence of experimental mixed-species infections on the expression of this pathology. Remarkably, the development of CM was completely inhibited by the simultaneous presence of P. yoelii yoelii but not that of P. vinckei or another line of P. berghei. In the protected coinfected mice, the accumulation of CD8+ T cells in the brain vasculature, a pivotal step in CM pathogenesis, was found to be abolished. Protection from CM was further found to be associated with species-specific suppression of PbA multiplication. These observations establish the concept of mixed Plasmodium species infections as potential modulators of pathology and open novel avenues to investigate mechanisms implicated in the pathogenesis of malaria.

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Pace, T., M. Ponzi, E. Dore, C. Janse, B. Mons, and C. Frontali. "Long insertions within telomeres contribute to chromosome size polymorphism in Plasmodium berghei." Molecular and Cellular Biology 10, no. 12 (December 1990): 6759–64. http://dx.doi.org/10.1128/mcb.10.12.6759.

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During prolonged in vivo mitotic multiplication of a Plasmodium berghei ANKA clone (8417HP), parasites that contained an enlarged version of chromosome 4 were observed. Restriction mapping and hybridization results demonstrated that the extra DNA present in the enlarged chromosome consists of 2.3-kb tandem repeats, known to be normally located in subtelomeric position at several chromosomal ends but absent in the original chromosome. The inserted 2.3-kb units appeared to interrupt one of the original telomeres and to create an internal (approximately 1-kb-long) telomeric sequence.

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Pace, T., M. Ponzi, E. Dore, C. Janse, B. Mons, and C. Frontali. "Long insertions within telomeres contribute to chromosome size polymorphism in Plasmodium berghei." Molecular and Cellular Biology 10, no. 12 (December 1990): 6759–64. http://dx.doi.org/10.1128/mcb.10.12.6759-6764.1990.

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During prolonged in vivo mitotic multiplication of a Plasmodium berghei ANKA clone (8417HP), parasites that contained an enlarged version of chromosome 4 were observed. Restriction mapping and hybridization results demonstrated that the extra DNA present in the enlarged chromosome consists of 2.3-kb tandem repeats, known to be normally located in subtelomeric position at several chromosomal ends but absent in the original chromosome. The inserted 2.3-kb units appeared to interrupt one of the original telomeres and to create an internal (approximately 1-kb-long) telomeric sequence.

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Hintsa, Gebretsadkan, Gereziher Geremedhin Sibhat, and Aman Karim. "Evaluation of Antimalarial Activity of the Leaf Latex and TLC Isolates from Aloe megalacantha Baker in Plasmodium berghei Infected Mice." Evidence-Based Complementary and Alternative Medicine 2019 (April 14, 2019): 1–9. http://dx.doi.org/10.1155/2019/6459498.

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Malaria is a devastating parasitic disease which caused around 216 million cases and 445,000 deaths worldwide in 2016. This might be attributed to a wide spread of drug resistant parasites. The plant Aloe megalacantha is indigenous to Ethiopia where the sap of the leaves is traditionally used for the treatment of malaria. This study was aimed at evaluating the antimalarial effect of leaf latex and isolates obtained from Aloe megalacantha against chloroquine sensitive Plasmodium berghei ANKA strain in Swiss albino mice. Peters’ 4-day suppressive test method was used to test the antimalarial activity of both leaves latex and isolates. Three isolates were obtained using thin layer chromatography and were coded as AM1, AM2, and AM3 in ascending order of their retention factor. After treatment of Plasmodium berghei infected mice with leaf latex of Aloe megalacantha for four days at 100, 200, and 400 mg/kg, it shows 30.3%, 43.4%, and 56.4% suppression of the parasite growth, respectively. 32.3%, 51.3%, and 67.4% chemosuppression after treatment with AM1, 39.8%, 50.6%, and 64.2% chemosuppression after treatment with AM2, and 52.6%, 69.4%, and 79.6% chemosuppression after treatment with AM3 were observed at doses of 100, 200, and 400 mg/kg/day, respectively. The observed parasite suppression of leaves latex and isolates was statistically significant (P<0.05) as compared to negative control. Moreover, both the leaves latex and isolates were also observed to prevent Plasmodium berghei induced body weight loss and hypothermia and increased the survival time of Plasmodium berghei infected mice as compared to the negative control. Hence, the present study supports the traditional claim of the plant for the treatment of malaria.

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Bonkian, Léa Nadège, R. Serge Yerbanga, Benjamin Koama, Aboubakar Soma, Mamoudou Cisse, Innocent Valea, Halidou Tinto, Jean Bosco Ouedraogo, T. Robert Guigemde, and Maminata Traore/Coulibaly. "In Vivo Antiplasmodial Activity of Two Sahelian Plant Extracts on Plasmodium berghei ANKA Infected NMRI Mice." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–4. http://dx.doi.org/10.1155/2018/6859632.

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Up to now, the control of malaria remains a challenge. The World Health Organization (WHO) recommends the use of artemisinin-based combination therapies (ACTs) for uncomplicated malaria treatment. Despite this guideline, many people in Burkina Faso use herbal medicine as primary treatment against malaria. The aim of this study was to assess the in vivo activity of Guiera senegalensis J. F. Gmel and Bauhinia rufescens Lam. leaves extracts against Plasmodium berghei ANKA. A four-day treatment of leaves decoction of each plant was administrated orally to 7 groups of six NMRI (Naval Medical Research Institute) mice infected with Plasmodium berghei ANKA strain. The control group received distilled water as treatment while the treated groups each received daily 100, 250, and 500 mg extract/kg body weight. Thin blood smears were performed on day five and the percentage of reduction of parasitaemia was determined compared to the control. The percentages of reduction of the parasitaemia at the doses of 100, 250, and 500 mg extract/kg body weight were, respectively, 57.5%, 35.9%, and 44.9% for Guiera senegalensis and 50.6%, 22.2%, and 25.7% for Bauhinia rufescens. Our findings on antiplasmodial activity of these two plants justify the traditional use by local populations against malaria. Thus, the isolation of the active compounds from these two plants is suggested for possible antimalarial candidate drugs.

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Nyandwaro, Kevin, Job Oyweri, Francis Kimani, and Amos Mbugua. "Evaluating Antiplasmodial and Antimalarial Activities of Soybean (Glycine max) Seed Extracts on P. falciparum Parasite Cultures and P. berghei-Infected Mice." Journal of Pathogens 2020 (February 18, 2020): 1–8. http://dx.doi.org/10.1155/2020/7605730.

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Background. Plasmodium parasite resistance to artemisinin-based combination therapies (ACTs) calls for development of new, affordable, safe, and effective antimalarial drugs. Studies conducted previously on soybean extracts have established that they possess antimicrobial, anti-inflammatory, anticancerous, and antioxidant properties. The activity of such extracts on Plasmodium parasites has not been potentially exploited. Objectives. The aim of this study was to determine the antiplasmodial activity of soybean extracts using Plasmodium falciparum cultures, followed by an in vivo evaluation of safety and antimalarial activity of the extracts in Plasmodium berghei ANKA strain-infected mice. Method. Aqueous, methanol, and peptide extracts of soybean seeds were prepared. An in vitro evaluation of the extracts for antiplasmodial activity was carried out using two P. falciparum strains: D6, a chloroquine-sensitive Sierra Leone 1 strain and W2, a chloroquine-resistant Indochina 1 strain. Following the in vitro assessment, two active extracts (peptide and methanol) were selected for in vivo assay with mice infected with P. berghei ANKA strain. The two extracts were tested for their therapeutic potential (curative test). The peptide extract was further assessed to determine whether it could prevent the establishment of a P. berghei infection (prophylactic test). For the curative tests, methanol and peptide extracts were separately administered orally to three groups of five P. berghei-infected Swiss albino mice for four days, at three dosage levels: 800, 400, and 200 mg/kg/day. In the prophylactic test, the similar dosage regimen was applied at baseline to 3 groups of uninfected mice using the peptide extract which was administered orally for 4 days. Results. Peptide and methanol extracts showed good activity with IC50 of 19.97 ± 2.57 μg/ml and 10.14 ± 9.04 μg/ml, respectively, against the D6 strain. The IC50 values for the peptide and methanol extracts were 28.61 ± 1.32 μg/ml and 14.87 ± 3.43 μg/ml, respectively, against the W2 strain. Methanol and peptide extracts exhibited high parasite-suppressive (therapeutic) activity of 72.9% and 71.9%, respectively, using the 800 mg/kg dose. In the prophylactic test, the peptide extract exhibited suppressive activity of 64.7% upon use of 800 mg/kg. Notably, there was a significant decrease (P<0.001) in suppression with lower doses. Conclusion. The results show the presence of antimalarial properties in soybean extracts with higher curative activity when compared to the prophylactic activity. However, more research needs to be conducted on this plant to possibly establish lead compounds.

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Carvalho, Leonardo JM, Maria F. Ferreira-da-Cruz, Claudio T. Daniel-Ribeiro, Marcelo Pelajo-Machado, and Henrique L. Lenzi. "Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice." Memórias do Instituto Oswaldo Cruz 101, no. 5 (August 2006): 523–28. http://dx.doi.org/10.1590/s0074-02762006000500007.

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Penet, Marie-France, Frank Kober, Sylviane Confort-Gouny, Yann Le Fur, Christiane Dalmasso, Nicolas Coltel, Agnès Liprandi, et al. "Plasmodium berghei ANKA infection causes brain damage in mice resistant to cerebral malaria." BMC Proceedings 2, Suppl 1 (2008): P55. http://dx.doi.org/10.1186/1753-6561-2-s1-p55.

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LANAR, D. "Sequence of the circumsporozoite gene of Plasmodium berghei ANKA clone and NK65 strain." Molecular and Biochemical Parasitology 39, no. 1 (February 1990): 151–53. http://dx.doi.org/10.1016/0166-6851(90)90018-h.

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Anyasor, God’swill Nduka, Isaac Olayinka Oyewole, Kayode Olushola Ogunwenmo, and Adegoke Ayowole. "Coartemether Induced Oxidative and Hepatic Damage in Plasmodium berghei Strain Anka Infected Mice." Bulletin of Environmental Contamination and Toxicology 88, no. 1 (November 6, 2011): 108–11. http://dx.doi.org/10.1007/s00128-011-0460-3.

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Adeyemi, O. I., O. O. Ige, M. A. Akanmu, and O. E. Ukponmwan. "In vivo anti-malarial activity of propranolol against experimental Plasmodium berghei ANKA infection in mice." African Journal of Clinical and Experimental Microbiology 21, no. 4 (August 25, 2020): 333–39. http://dx.doi.org/10.4314/ajcem.v21i4.10.

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Background: Malaria is a mosquito-borne infectious disease caused by Plasmodium spp, which is widespread in tropical and subtropical regions of the world. The objective of this study is to evaluate in vivo antimalarial activity of propranolol against experimental Plasmodium berghei ANKA (PbA) infection in a mouse model.Methods: A total of 36 mice weighing between 15 to 18g were randomly divided into six groups of six mice each. Mice in the first group (SAL) were non-infected with P. berghei but received normal saline (control), second group (PbA) were mice infected without treatment (control), third group (PRL) were non-infected mice treated with propranolol at the dose of 7.5 mg/kg/bid, fourth group (PbA+PRL) were mice infected and treated with same dose of propranolol, fifth group (QUN) were non-infected mice treated with quinine at a dose of 20 mg/kg stat, then 10 mg/kg bid, and sixth group (PbA+QUN) were infected mice treated with quinine. Parasitaemia, physiological conditions (cognitive function, temperature) and lethality of infected mice were monitored over 7-day period to assess the antimalarial activity of propranolol and quinine. The Y-maze paradigm was used to assess cognitive impairment induced by PbA infection. The effects of propranolol on malaria indices and cognitive impairment were compared with that of quinine and the control using T-test statistical method.Results: Mortality of mice at day 7 in the infected group without treatment (PbA) was 100% (6/6) while mortality was 50% (3/6) in infected group treated with propranolol (PbA+PRL) and 33.3% (2/6) in infected group treated with quinine (PbA+QUN) (OR=2.000, p=1.000). No mortality was recorded in any of the three groups of uninfected mice. Propranolol reduced parasitaemia to a trough level of 1.40±0.07 three days after treatment, comparable to trough level of 1.39±0.0633 by quinine but did not reverse PbA-induced hypothermia, which quinine did.Conclusion: Propranolol demonstrated in vivo antimalarial activity against experimental PbA infection in mice comparable to that of quinine. Keywords: malaria, propranolol, quinine, Plasmodium, cerebral malaria French Title: Activité antipaludique in vivo du propranolol contre l'infection expérimentale par Plasmodium berghei ANKA chez la souris Contexte: Le paludisme est une maladie infectieuse transmise par les moustiques causée par Plasmodium spp, qui est répandue dans les régions tropicales et subtropicales du monde. L'objectif de cette étude est d'évaluer l'activité antipaludique in vivo du propranolol contre une infection expérimentale à Plasmodium berghei ANKA (PbA) dans un modèle murin. Méthodes: Un total de 36 souris pesant entre 15 et 18 g ont été réparties au hasard en six groupes de six souris chacun. Les souris du premier groupe (SAL) n'étaient pas infectées par P. berghei mais ont reçu une solution saline normale (contrôle), le deuxième groupe (PbA) était des souris infectées sans traitement (contrôle), le troisième groupe (PRL) était des souris non infectées traitées par propranolol à la dose de 7,5mg/kg/bid, le quatrième groupe (PbA+PRL) étaient des souris infectées et traitées avec la même dose de propranolol, le cinquième groupe (QUN) étaient des souris non infectées traitées avec de la quinine à une dose de 20mg/kg stat, puis 10mg/kg bid et le sixième groupe (PbA+QUN) étaient des souris infectées traitées avec de la quinine. La parasitémie, les conditions physiologiques (fonction cognitive, température) et la létalité des souris infectées ont été surveillées sur une période de 7 jours pour évaluer l'activité antipaludique du propranolol et de la quinine. Le paradigme du labyrinthe en Y a été utilisé pour évaluer les troubles cognitifs induits par l'infection au PbA. Les effets du propranolol sur les indices du paludisme et les troubles cognitifs ont été comparés à ceux de la quinine et du témoin à l'aide de la méthode statistique du test T. Résultats: La mortalité des souris au jour 7 dans le groupe infecté sans traitement (PbA) était de 100% (6/6) tandis que la mortalité était de 50% (3/6) dans le groupe infecté traité avec du propranolol (PbA+PRL) et 33,3% ( 2/6) dans le groupe infecté traité par la quinine (PbA+QUN) (OR=2.000, p=1.000). Aucune mortalité n'a été enregistrée dans aucun des trois groupes de souris non infectées. Le propranolol a réduit la parasitémie à un niveau minimum de 1,40±0,07 trois jours après le traitement, comparable au niveau minimum de 1,39±0,0633 de la quinine, mais n'a pas inversé l'hypothermie induite par le PbA, ce que la quinine a fait. Conclusion: le propranolol a démontré une activité antipaludique in vivo contre l'infection expérimentale au PbA chez la souris comparable à celle de la quinine. Mots-clés: paludisme, propranolol, quinine, Plasmodium, paludisme cérébral

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Wardani, Kartika Arum, Kholida Nur Aini, Heny Arwati, and Willy Sandhika. "Sequestration of erythrocytes infected with Plasmodium berghei ANKA in BALB/c mice treated with goat bile." Qanun Medika - Medical Journal Faculty of Medicine Muhammadiyah Surabaya 4, no. 2 (July 29, 2020): 179. http://dx.doi.org/10.30651/jqm.v4i2.3539.

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Abstract Sequestration of Plasmodium berghei ANKA-infected erythrocytes occurs in BALB/c mice as characteristic of Plasmodium falciparum infection in humans. Animals’ bile has been widely used for centuries in Traditional Chinese Medicine. Goat bile has been used in healing infectious and non-infectious diseases; however, no report on the use of goat bile against malaria infection and sequestration. The purpose of this study was to analyze the correlation between parasitemia and sequestration in the liver of P.berghei ANKA-infected BALB/c mice treated with goat bile. This research was an in vivo experimental study using the post-test control group design. The male BALB/c mice aged ± 6 weeks, body weight 20-25 g were used. The mice were divided into five groups where Group 1-3 were mice treated with goat bile 25%, 50%, and 100%, respectively. Group 4-5 were negative (sterile water) and positive controls (DHP). Parasitemia was observed daily from each mouse and the number of sequestered infected erythrocytes on the endothelium of sinusoids. The data were analyzed using t independent test. Antimalarial activity of goat bile was shown by the lower parasitemia in goat bile-treated mice compared with the negative control. The average number of sequestration was goat bile concentration-dependent manner. The higher the concentration, the lower the number of sequestration. Sequestration was correlated with parasitemia (p=0,0001). Sequestration of P.berghei ANKA-infected erythrocytes correlated with parasitemia, and was goat bile concentration-dependent manner. Keywords: Malaria, parasitemia, sequestration, goat bileCorrespondence: arwatiheny@gmail.com

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Ounjaijean, Sakaewan, Manas Kotepui, and Voravuth Somsak. "Antimalarial Activity of Tinospora baenzigeri against Plasmodium berghei-Infected Mice." Journal of Tropical Medicine 2019 (September 5, 2019): 1–6. http://dx.doi.org/10.1155/2019/5464519.

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Plant species of the genus Tinospora (Menispermaceae) possess several pharmacological properties, and T. crispa has been reported to have antimalarial activity. T. baenzigeri (Chingcha Chalee) is a rich source of terpenes and quinoline alkaloids; however, it still has not yet been investigated the antimalarial activity of this plant extract. Hence, this study was aimed to evaluate the antimalarial activity of T. baenzigeri stem extract against Plasmodium berghei-infected mice. The aqueous crude extract of T. baenzigeri stem was prepared using a microwave-assisted method and tested for acute toxicity in mice. For evaluating the antimalarial activity in vivo, the standard 4-day test was carried out using groups of ICR mice infected with P. berghei ANKA administered orally by gavage with the extract (100, 250, and 500 mg/kg) for 4 consecutive days. Parasitemia, body weight, packed cell volume, and mean survival time were then measured. It was found that the aqueous crude extract of T. baenzigeri stem did not exhibit any sign of toxicity up to the dose of 2,000 mg/kg. The extract significantly (P<0.01) inhibited parasitemia in a dose-dependent manner, with 22.02%, 50.81%, and 74.95% inhibition. Moreover, the marked prevention of body weight loss and packed cell volume reduction was observed at doses of 100, 250, and 500 mg/kg of extract-treated mice. Additionally, the extract prolonged the mean survival time of P. berghei-infected mice, compared to the untreated group. In conclusion, the aqueous crude extract of T. baenzigeri stem has demonstrated potent antimalarial activity against P. berghei-infected mice with prolonged mean survival time and prevention of body weight loss and packed cell volume reduction.

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Colmenarez, Custodiana, María Acosta, Miguel Rodríguez, and Jaime Charris. "Synthesis and antimalarial activity of (S)-methyl-(7-chloroquinolin-4-ylthio)acetamidoalquilate derivatives." Journal of Chemical Research 44, no. 3-4 (December 10, 2019): 161–66. http://dx.doi.org/10.1177/1747519819890559.

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The synthesis of five new ( S)-methyl-(7-chloroquinolin-4-ylthio)acetamidoalquilate derivatives is carried out under a modified version of the Steglich esterification reaction between different l-amino acid methyl esters and 2-(7-chloroquinolin-4-ylthio)acetic acid. Two of the compounds showed significant inhibition (>50%) of β-hematin formation. The two active structures were tested in vivo as potential antimalarials in mice infected with Plasmodium berghei ANKA, a chloroquine susceptible strain. Compounds 6b and 6e exhibited antimalarial activity comparable to that of chloroquine.

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Ali, Amatul Hamizah, Suhaini Sudi, Ng Shi-Jing, Wan Rozianoor Mohd Hassan, Rusliza Basir, Hani Kartini Agustar, Noor Embi, Hasidah Mohd Sidek, and Jalifah Latip. "Dual Anti-Malarial and GSK3β-Mediated Cytokine-Modulating Activities of Quercetin Are Requisite of Its Potential as a Plant-Derived Therapeutic in Malaria." Pharmaceuticals 14, no. 3 (March 9, 2021): 248. http://dx.doi.org/10.3390/ph14030248.

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Although death in malaria is attributed to cerebrovascular blockage and anaemia, overwhelming cytokine production can contribute to the severity of the disease. Therefore, mitigation of dysregulated inflammatory signalling may provide further benefit for malaria treatment. Quercetin (3,3′,4′,5,7-pentahydroxyflavone) is known to inhibit glycogen synthase kinase-3β (GSK3β), a potent regulator of both pro- and anti-inflammatory effects. Quercetin is therefore a potential therapeutic to modulate the imbalanced cytokine production during malarial infection. Anti-malarial effects of quercetin were evaluated in murine models of severe and cerebral malaria using Plasmodium berghei NK65 and ANKA strains, respectively. Western blotting and analysis of cytokines were carried out to determine the GSK3β-mediated cytokine-modulating effects of quercetin in infected animals. Quercetin (25 mg/kg BW) treatment in P. berghei NK65-infected animals resulted in 60.7 ± 2.4% suppression of parasitaemia and significantly decreased serum levels of TNF-α and IFN-γ, whilst levels of IL-10 and IL-4 were elevated significantly. Western analysis revealed that pGSK3β (Ser9) increased 2.7-fold in the liver of quercetin-treated NK65-infected animals. Treatment of P. berghei ANKA-infected mice with quercetin (15 mg/kg BW) increased (2.3-fold) pGSK3β (Ser9) in the brains of infected animals. Quercetin is a potential plant-derived therapeutic for malaria on the basis that it can elicit anti-malarial and GSK3β-mediated cytokine-modulating effects.

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Raymond Bess Bila, Germain Sotoing Taiwe, David Denis Feugaing Sofeu, Orelien Sylvain Mtopi Bopda, Hart Mann Alain Youbi Mambou, Seraphin Nji Ombel Musa, Liliane Laure Toukam, and Helen Kuokuo Kimbi. "Prophylactic antimalarial effects of Cymbopogon citratus (DC.) Stapf (Poaceae) in a mouse model of Plasmodium berghei ANKA infection: normalisation of haematological and serum biochemical status." GSC Biological and Pharmaceutical Sciences 15, no. 1 (April 30, 2021): 05–017. http://dx.doi.org/10.30574/gscbps.2021.15.1.0084.

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Ethnopharmacological relevance: Cymbopogon citratus (DC.) Stapf (Poaceae) is a medicinal plant known for its antimalarial, antipyretic and antifatigue activities in Cameroonian folk medicine. Aim of the study: The aim of this work was to evaluate the prophylactic antimalarial effects of the decoction prepared from the leaves of Cymbopogon citratus on Plasmodium berghei ANKA infection in mice and investigate its action on haematological and serum biochemical status. Materials and methods: Swiss mice were treated with Cymbopogon citratus leaf decoction (25, 50, 100 and 200 mg/kg) and later inoculated with Plasmodium berghei ANKA. The prophylactic antimalarial activity of the decoction was evaluated by determining the parasitaemia, percentage chemosuppression, body weight, body temperature, food and water intake in pretreated parasitised mice. The possible ameliorative effects of the decoction on malaria associated haematological and serum biochemical changes were also assessed. Results: The decoction exhibited a prophylactic activity of 85.32% and its chemotherapeutic effects ranged from 56.88 – 85.32% with maximum effect observed at the highest experimental dose. It significantly inhibited parasitaemia (P < 0.001) compared to the negative control group. Interestingly, treatment of parasitised mice with the decoction significantly restored the malaria modified haematological and biochemical status compared with distilled water-treated parasitised mice. Conclusion: The results of this prophylactic assay indicated that Cymbopogon citratus decoction has antimalarial effects and normalised haematological and serum biochemical aberrations generated by malaria. Hence, Cymbopogon citratus represents a promising source of new antimalarial agents.

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Journal articles on the topic 'Plasmodium berghei ANKA'

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