Expression data from malaria-specific mouse CD4 T cell (PbT-II) subset after Plasmodium berghei ANKA infection
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PROVIDER: PRJNA745347 | ENA |
REPOSITORIES: ENA
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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. Keywords: disease state analysis
2007-10-11 | GSE6019 | GEO
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
Project description:Characterization of Neuropilin-1+ and Neuropilin-1- splenic CD8+ T cells from Plasmodium berghei ANKA-infected C57BL/6 mice
2022-12-31 | GSE199569 | GEO
Project description:The multiple species of Plasmodium that infect humans are highly polymorphic and induce various infections ranging from asymptomatic state to severe life-threatening diseases such as cerebral malaria. However, how the differences between the parasites affect host immune responses during blood-stage infection remains largely unknown. In this study, we investigated the CD4+ T-cell immune responses in T-cell receptor-transgenic mice infected simultaneously with P. berghei ANKA (PbA) and P. chabaudi chabaudi AS (Pcc) using PbT-II cells, which recognize a common epitope of these parasites. In the acute phase of infection, CD4+ T-cell responses in PbA-infected mice showed a higher involvement of Th1 cells and a lower proportion of Ly6Clo effector CD4+ T cells than those in Pcc-infected mice. Transcriptome analysis of PbT-II cells indicated that type I interferon (IFN)-regulated genes were expressed at higher levels in both Th1- and Tfh-type PbT-II cells from PbA-infected mice than those from Pcc-infected mice. Moreover, IFN-α levels were considerably higher in PbA-infected mice than in Pcc-infected mice. Inhibition of type I IFN signaling increased PbT-II and Ly6Clo cell numbers and partially reversed the Th1 over Tfh bias of the PbT-II cells in both PbA- and Pcc-infected mice. However, in the memory phase, we did not find a significant difference in the phenotype of PbT-II cells between PbA- and Pcc-primed mice. These observations suggested that the differences in Plasmodium-specific CD4+ T-cell responses between PbA- and Pcc-infected mice were at least partially associated with the difference in type I cytokine production during the early phase of the infection.
2021-07-11 | GSE179860 | GEO
Project description:Comparative analysis of the rodent malaria genome Plasmodium berghei ANKA
| PRJEB5710 | ENA
Project description:Recent advances in high throughput sequencing methodologies allow the opportunity to probe in depth the transcriptomes of organisms including important human pathogens. In this project, we are using Illumina sequencing technology to analyze the transcriptome (RNA-Seq) of experimentally accessible stages of the mouse malaria parasite, P. berghei ANKA. The aim is to make transcriptional landscape maps of different life cycle stages of P. berghei ANKA at single base pairs resolution. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2014-02-21 | E-ERAD-250 | biostudies-arrayexpress
Project description:We have used cDNA microarrays to compare gene expression profiles in brains from normal mice to those infected with the Anka strain of Plasmodium berghei, a model of cerebral malaria. For each of three brains in each group, we computed ratios of all quantifiable genes with a composite reference sample and then computed ratios of gene expression in infected brains with untreated controls. Of the almost 12,000 unigenes adequateluy quantified in all arrays, about 3% were significantly downregulated (p<0.05, >50% fold change) and about 7% were upregulated. Upon inspection of the lists of regulated genes, we identified a high number encoding proteins of importance to normal brain function or associated with neuropathology. These results emphasize the important impact of malarial infection on gene expression in brain and provide tentative target biomarkers that might provide novel therapeutic targets for neurological sequelae of disease.
2010-09-17 | GSE24086 | GEO
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
Project description:We use the Plasmodium berghei rodent model to characterize the proteome of the final phase of liver stage development, the merosomes, packets of hepatic merozoites that bud from the host hepatocyte to initiate the blood stage of malaria. Plasmodium berghei WT ANKA strain was used to infect HepG2 hepatoma cells. Samples were fractionated by strong cation exchange, and nano-LC Orbitrap mass spectrometry was used to perform untargeted proteomic profiling of 3 biological replicates. Data was processed using MaxQuant and LFQ. Additional searches were performed to identify peptides from cleaved acetylated PEXELs (protein export elements) to identify proteins putatively exported to the host hepatocyte during liver stage development.
2019-03-25 | PXD010559 | Pride
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