Pathology of malaria in West Africa.

Edington, G. M.

doi:10.1136/bmj.1.5542.715

Cited by 110 publications

(36 citation statements)

References 20 publications

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“…Perivascular mononuclear cell infiltration was observed in the livers of infected treated mice with CQ, MJ 25 and 50 mg/kg, while necrosis was observed in the livers of untreated group. However, livers of infected mice treated with AE were normal, which supports the report of Edington 17 . Gilles et al 18 reported that changes in histopathology occur if P. berghei penetrate the cerebrum.…”

Section: Figure 4 Effect Of Treatment On Lipid Profiles In Various Grsupporting

confidence: 88%

Potential antimalarial activity of Methyl Jasmonate and its effect on lipid profiles in Plasmodium Berghei infected mice

et al. 2015

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Background: The antimalarial activity and lipid profiles of Methyl Jasmonate (MJ) were investigated against established malaria infection in vivo using BALB/c mice. Methods: Arteether (AE) and chloroquine (CQ) were used as reference drugs while ethanol was used as the vehicle for drug delivery for MJ. Results: Mice treated with 10 and 25 mg/kg MJ showed a remarkable reduction in percentage parasitemia by 68.3% and 78.2% on day 10(post treatment) respectively while 45.4% and 87.2% reduction in percentage parasitemia were observed in the group treated with 50 mg/kg on day 3 and 10 ( post treatment ) respectively. The highest mean survival time was observed in CQ followed by AE and MJ in dose-dependent manner. A progressive decrease in packed cell volume (PCV) was observed in infected untreated mice which led to the death of all the mice by day 9 (post treatment). Infected mice treated with MJ showed reduced level of HDL and LDL compared with infected untreated group. As the dose of MJ increased in infected mice cholesterol levels increased while there was reduction in triglyceride. Conclusion: Overall there was marked decrease in parasitemia in Plasmodium berghei infected mice treated with graded doses of MJ but appears to have reduced antimalarial activity compared with CQ and AE.

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Section: Figure 4 Effect Of Treatment On Lipid Profiles In Various Grsupporting

confidence: 88%

Potential antimalarial activity of Methyl Jasmonate and its effect on lipid profiles in Plasmodium Berghei infected mice

et al. 2015

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“…into the tail vein of BALB/c mice. sHZ effects were monitored in the liver because its accumulation in this organ has been associated with infection chronicity in humans (39), and with cumulative parasite burden and duration of infection in experimental malaria (40). The various concentrations were chosen based on previous studies performed by Sherry et al (22), who, by reference to standard hematological measurements, estimated that as much as 200 mol of HZ (ϳ3 mol/Kg) is released into the circulation of a 70 kg P. falciparum-infected human patient who has a 1% synchronized parasitemia.…”

Section: Shz Induces Liver Chemokine and Cytokine Mrna Expressionmentioning

confidence: 99%

Hemozoin-Inducible Proinflammatory Events In Vivo: Potential Role in Malaria Infection

Jaramillo

Plante

Ouellet

et al. 2004

The Journal of Immunology

123

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During malaria infection, high levels of proinflammatory molecules (e.g., cytokines, chemokines) correlate with disease severity. Even if their role as activators of the host immune response has been studied, the direct contribution of hemozoin (HZ), a parasite metabolite, to such a strong induction is not fully understood. Previous in vitro studies demonstrated that both Plasmodium falciparum HZ and synthetic HZ (sHZ), β-hematin, induce macrophage/monocyte chemokine and proinflammatory cytokine secretion. In the present study, we investigated the proinflammatory properties of sHZ in vivo. To this end, increasing doses of sHZ were injected either i.v. or into an air pouch generated on the dorsum of BALB/c mice over a 24-h period. Our results showed that sHZ is a strong modulator of leukocyte recruitment and more specifically of neutrophil and monocyte populations. In addition, evaluation of chemokine and cytokine mRNA and protein expression revealed that sHZ induces the expression of chemokines, macrophage-inflammatory protein (MIP)-1α/CCL3, MIP-1β/CCL4, MIP-2/CXCL2, and monocyte chemoattractant protein-1/CCL2; chemokine receptors, CCR1, CCR2, CCR5, CXCR2, and CXCR4; cytokines, IL-1β and IL-6; and myeloid-related proteins, S100A8, S100A9, and S100A8/A9, in the air pouch exudates. Of interest, chemokine and cytokine mRNA up-regulation were also detected in the liver of i.v. sHZ-injected mice. In conclusion, our study demonstrates that sHZ is a potent proinflammatory agent in vivo, which could contribute to the immunopathology related to malaria.

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“…However, the observation of this phenomenon in non-CM cases (29) suggested that other factors are involved. The first evidence of leukocyte involvement in HCM pathogenesis came from the observation that individuals suffering from thymic abnormality were protected from severe malaria (11). Moreover, leukocytes were detected in the brains of patients that had died of CM (25,31).…”

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confidence: 99%

Accumulation ofPlasmodium berghei-Infected Red Blood Cells in the Brain Is Crucial for the Development of Cerebral Malaria in Mice

et al. 2010

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Cerebral malaria is the most severe complication of human infection with Plasmodium falciparum. It was shown that Plasmodium berghei ANKA-induced cerebral malaria was prevented in 100% of mice depleted of CD8 ؉ T cells 1 day prior to the development of neurological signs. However, the importance of parasites in the brains of these mice was never clearly investigated. Moreover, the relevance of this model to human cerebral malaria has been questioned many times, especially concerning the relative importance of leukocytes versus parasitized erythrocytes sequestered in the brain. Here, we show that mice protected from cerebral malaria by CD8 ؉ T-cell depletion have significantly fewer parasites in the brain. Treatment of infected mice with an antimalarial drug 15 to 20 h prior to the estimated time of death also protected mice from cerebral malaria without altering the number of CD8 ؉ T cells in the brain. These mice subsequently developed cerebral malaria with parasitized red blood cells in the brain. Our results clearly demonstrated that sequestration of CD8 ؉ T cells in the brain is not sufficient for the development of cerebral malaria in C57BL/6 mice but that the concomitant presence of parasitized red blood cells is crucial for the onset of pathology. Importantly, these results also demonstrated that the experimental cerebral malaria model shares many features with human pathology and might be a relevant model to study its pathogenesis.Malaria causes 1 million deaths per year, most of them due to cerebral malaria (CM) induced by infection with Plasmodium falciparum. The precise mechanism responsible for this neuropathology remains far from being fully understood. Cytoadherence of parasitized red blood cells (pRBC) to endothelial cells of the cerebral microvasculature in P. falciparum-infected people has been implicated as the major process responsible for development of human CM (HCM) (5,20,30). However, the observation of this phenomenon in non-CM cases (29) suggested that other factors are involved. The first evidence of leukocyte involvement in HCM pathogenesis came from the observation that individuals suffering from thymic abnormality were protected from severe malaria (11). Moreover, leukocytes were detected in the brains of patients that had died of CM (25, 31). Also, histological analysis of brains from Malawian children that had died of CM revealed an important accumulation of intravascular leukocytes and platelets compared with brains of children dying of other complications of malaria (9, 15).Infection of the malaria-susceptible C57BL/6 mouse strain with Plasmodium berghei ANKA provides an experimental model of CM that shares some characteristics with HCM and has been extensively used to dissect the mechanisms involved in CM (reviewed in reference 28). While pRBC sequestration has been demonstrated for P. falciparum, it remains to be clearly shown in experimental CM (ECM). Nevertheless, recent studies have shown that P. berghei ANKA can be sequestered in vivo in different organs, including the brai...

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Pathology of malaria in West Africa.

Cited by 110 publications

References 20 publications

Potential antimalarial activity of Methyl Jasmonate and its effect on lipid profiles in Plasmodium Berghei infected mice

Potential antimalarial activity of Methyl Jasmonate and its effect on lipid profiles in Plasmodium Berghei infected mice

Hemozoin-Inducible Proinflammatory Events In Vivo: Potential Role in Malaria Infection

Accumulation ofPlasmodium berghei-Infected Red Blood Cells in the Brain Is Crucial for the Development of Cerebral Malaria in Mice

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