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RNA-seq analysis of anti-malarial drug chemotherapy of murine experimental Cerebral Malaria (ECM)

ABSTRACT: RNA-seq analysis of anti-malarial drug chemotherapy of murine experimental Cerebral Malaria (ECM)

PROVIDER: PRJEB24903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2287680_1.fastq.gz	Fastqsanger.gz
	ERR2287680_2.fastq.gz	Fastqsanger.gz
	ERR2287690_1.fastq.gz	Fastqsanger.gz
	ERR2287690_2.fastq.gz	Fastqsanger.gz
	ERR2287700_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of anti-malarial drug chemotherapy of murine experimental Cerebral Malaria (ECM)

Project description:Cerebral Malaria (HCM) is a serious neurological complication caused by Plasmodium falciparum infection. Currently the only treatment for HCM is the provision of anti-malarial drugs; however, such treatment by itself often fails to prevent death or development of neurological sequelae. To identify new potential adjunct treatments for HCM, we performed a non-biased whole brain transcriptomic time-course analysis of anti-malarial drug chemotherapy of murine experimental CM (ECM).

2018-07-03 | E-MTAB-6474 | biostudies-arrayexpress

Infection-induced resistance to experimental cerebral malaria

Project description:Cerebral malaria (CM) is one of the most severe complications of malaria infection. There is evidence that repeated parasite exposure promotes resistance against CM, as indicated by the low incidence of CM in adults in malaria-endemic regions. However, the immunological basis of this infection-induced resistance remains poorly understood. Here, a microarray study done utilising the tractable Plasmodium berghei ANKA model of experimental cerebral malaria (ECM), we show that three rounds of infection and drug-cure protects against the development of ECM during a subsequent fourth infection.

2019-02-19 | E-MTAB-5513 | biostudies-arrayexpress

Transcriptomic profiling of microglia from a model of Experimental Cerebral Malaria Transcriptomic profiling of microglia from a model of Experimental Cerebral Malaria

Project description:Cerebral malaria is a pathology involving inflammation in the brain. There are many immune cell types activated during this process, but there is little information on the contribution of microglia, the brain resident macrophages, to this severe complication. We have examined the responses of microglia in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA. Genome wide transcriptomic analysis of these cells revealed that thousands of transcripts were differentially expressed at two different time points during the infection. The analysis indicated that proliferation of microglia was a dominant feature before the onset of ECM, and supporting this, we observed an increase in numbers of these cells in the brain. When cerebral malaria symptoms were manifest, genes involved in immune responses and chemokine production were upregulated, which were possibly driven by Type I Interferon. Together, our data offer a unique insight into the responses of microglia in the brain during ECM.

2016-12-19 | GSE86082 | GEO

Transcriptional Profiling of Cerebral Malaria

Project description:Cerebral malaria (CM) is a leading cause of death in the world. Better understanding of the pathogenesis of this disease is critical for the development of novel therapies. In this work, we investigated temporal gene expression profiles in the brains of CM-susceptible and CM-resistant mice during infection with P. Berghia ANKA (PbA). In this model of CM, susceptible mice develop neurological signs by day 6 post infection while resistant mice do not develop neurological manifestations during malarial infection. Keywords: Time course

2007-10-01 | GSE7814 | GEO

RNA-seq analysis of the mouse brain reveals inflammatory genes associated with early artesunate treatment of experimental cerebral malaria

Project description:Purpose:This study aimed to investigate the transcriptome-wide response of experimental cerebral malaria (ECM) and artesunate treated mice brain on 6 days post-infection. Methods: C57BL/6 mice were infected with Plasmodium berghei ANKA to construct a murine ECM in MB and AB group. AB group treated with artesunate (30mg/kg), while CB group treated with PBS for 4 days. Mice brain was tested by RNA-seq. Results: Gene ontology and KEGG pathway analyses of differentially expressed genes (DEGs) were performed. quantitative reverse transcription polymerase chain reaction (qPCR) verify DEGs such as Il6, Il1b, Il10, Tnf, Ifng, Il21, Icam1, which were up-regulated in MB vs. CB, while down-regulated in AB vs. MB. Conclusions:Our study revealed a transcriptome-wide profile in ECM and artesunate treated mice brain, and help to explore the underlying mechanism, as well as the further development of therapeutic strategies for clinical cerebral malaria.

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Distinct pathways of pathogenesis in mice with experimental cerebral malaria following P. berghei ANKA infection.

2007-10-11 | GSE6019 | GEO

Transcription profiling of mouse with experimental cerebral malaria following P. berghei ANKA infection.

Project description:Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, predominantly experienced by children and non-immune adults, which results in great mortality and long-term sequelae. Recent reports based on histology of post-mortem brain tissue suggest that CM may be the common end point for a range of syndromes. Here, we have analysed the gene expression profiles in brain tissue taken from experimental CM (ECM)-susceptible, Plasmodium berghei ANKA (PbA)-infected C57BL/6 (B6) and CBA/CaH (CBA) mice with ECM. Gene expression profiles were largely heterogeneous between the two ECM-susceptible strains. These results, combined with experimental data, support the existence of distinct pathogenic pathways in CM. Experiment Overall Design: C57BL/6 and CBA/CaH mice were infected with 10e5 Plasmodium berghei ANKA-infected RBCs and monitored for ECM development. At onset of ECM symptoms, infected mice and naive controls were culled, perfused (in order to remove non-adherent circulating cells), and brains were removed. Total RNA was extracted from these brains and pooled (n=6 mice/ group). Pooled RNA samples were converted to cDNA and antisense cRNA, labelled and hybridized to GeneChip Mouse Genome 430 2.0 Arrays (Affymetrix, Surrey Hills, Australia). Arrays were scanned using the GeneChip Scanner 3000 (Affymetrix) and GeneChip Operating Software v1.1.1 (Affymetrix). Normalisation and initial analyses were carried out in GeneSpring v7 (Agilent Technologies). Values below 0.01 were set to 0.01. Each measurement was divided by the 50th percentile of all measurements in that sample. The data was filtered for genes flagged as present, which had at least an expression level of 50. Following this, a threshold of 2.5 fold up-regulation or down-regulation of genes differentially expressed during ECM was set.

2008-06-14 | E-GEOD-6019 | biostudies-arrayexpress

Transcription profiling of genetically cerebral malaria-resistant (CM-R) and cerebral malaria-susceptible (CM-S) mouse strains

Project description:Gene expression patterns were investigated in well-defined genetically cerebral malaria-resistant (CM-R) and cerebral malaria-susceptible (CM-S) mouse strains. cDNA microarrays were used to search for differentially expressed genes in mouse brain. Four mouse strains, known to differ in susceptibility to cerebral malaria upon Plasmodium berghei ANKA infection, were compared: BALB/c and DBA/2 mice are CM-R, while C57BL/6 and CBA/J mice are CM-S.

2005-06-30 | E-MEXP-370 | biostudies-arrayexpress

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2008-06-15 | E-GEOD-7814 | biostudies-arrayexpress

Cerebral malaria is regulated by host mediated changes in Plasmodium gene expression

Project description:Cerebral Malaria (CM), the deadliest complication of Plasmodium infection, is a complex and unpredictable disease. Currently, our understanding of the factors that trigger progression of malaria to CM is limited. Here, by infecting experimental CM (ECM) resistant (Balb/c) and ECM susceptible (C57BL/6) mice with ECM causing (ANKA) and non-ECM causing (NK65) Plasmodium berghei (Pb) parasite strains, we revealed that in resistant host, infection by ECM causing parasite develops similar to infection by non-ECM causing parasite in susceptible host in terms of parasite growth in host, disease course and host immune response against parasite. Our comparative gene expression analysis revealed that in Balb/c host, gene expression of Pb ANKA parasite is remarkably different from, the gene expression of Pb ANKA in C57BL/6 but similar to the gene expression of non-ECM causing Pb NK65 in C57BL/6. Thus, host has a critical influence on parasite behavior which ultimately determines the course of malaria disease.

2023-02-21 | GSE215359 | GEO

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