Simultaneous Host and Parasite Expression Profiling Identifies Transcriptional Programs Associated with Cerebral Malaria
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE5672
PROVIDER: PRJNA96953 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The development and outcome of cerebral malaria (CM) reflects a complex interplay between parasite-expressed virulence factors and host response to infection. To simultaneously analyze transcriptional programs in both parasite and host over the course of infection, we created microarrays to concurrently detect transcripts in the genomes of both Plasmodium berghei and mouse. Analysis of RNA from brain, lung, liver, and spleen of mice infected with P. berghei ANKA showed that parasite gene expression is readily detected in whole organ RNA. Comparison of CM-susceptible (C57BL/6) and CM-resistant (BALB/c) mice showed that both host and parasite display distinct organ-specific transcriptional signatures in susceptible versus resistant animals. Host genes whose expression differs between CM-resistant and CM-susceptible mice, at either baseline or induced by infection, tend to relate to humoral and immune response, complement activation, or cell-cell interactions, suggesting differences in immune function that may directly underlie protection from or susceptibility to CM. P. berghei, in contrast, displayed differential expression of genes related to apparent biosynthestic activities, with the majority of transcriptional activity observed in the lung. These data show that analysis of host and parasite gene expression profiles by hybridizing infected host samples to a single microarray is feasible, and can facilitate dissection of complex host-pathogen interactions. Keywords: Time course, Disease state analysis
2006-11-24 | GSE5672 | GEO
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
Project description:We have shown previously (Reid & Berriman, NAR, 2012) that by simultaneously examining host and parasite gene expression over the course of infection we can determine pairs of genes involved in host-parasite interaction. Here we are producing a high quality dataset which will specifically allow us to exploit this finding to identify genes involved in malaria host-parasite interaction. This has been done in collaboration with Jean Langhorne at NIMR. 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/
2013-05-13 | E-ERAD-136 | biostudies-arrayexpress
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: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
Project description:Rodent malaria parasite RNA hybridized on Illumina Mouse WG-6 v2.0 Expression BeadChip To investigate whether parasite RNA interfere with mouse beadchip analaysis. Malaria parasite resides in red blood cell, therefore RNA isolated from whole infected blood contains host RNA as well as parasite RNA
2020-04-30 | GSE145634 | GEO
Project description:We hypothesized that differential gene expression contributes to phenotypic variation of parasites which results in specific interaction of Plasmodium falciparum with its human host. In this study we used microarray hybridization to analyse the transcriptomes of P.falciparum isolated from asymptomatic carriers and from cerebral and uncomplicated malaria patients. We also investigated the transcriptomes of the 3D7 clone and the selected 3D7-Lib line.
2014-12-01 | E-MTAB-2139 | biostudies-arrayexpress
Project description:Replication origin mapping in the malaria parasite Plasmodium falciparum
2022-08-04 | GSE210010 | GEO
Project description:Cerebral malaria is the most deadly manifestation of infection with Plasmodium falciparum. The pathology of cerebral malaria is characterised by the accumulation of infected erythrocytes in the microvasculature of the brain, due to parasite adhesins on the surface of infected erythrocytes binding to human receptors on microvascular endothelial cells. The parasite and host molecules involved in this interaction are unknown. We used the Human Brain Endothelial Cell line HBEC-5i to identify the malaria parasite ligands responsible for binding to human brain endothelial cells. Three P. falciparum strains (HB3, 3D7 and IT/FCR3) were selected for binding to HBEC5i and the whole transcriptome of selected and unselected parasites was analysed using a variant surface antigen-supplemented microarray chip. After selection, the only highly upregulated genes were a subset of group A-like var genes (HB3var3, 3D7_PFD0020c, ITvar7 and ITvar19), that showed 11 to >100-fold higher transcription levels in selected parasites. These genes are highly diverse in sequence, but do however show strong similarities in PfEMP1 architecture. Antibodies raised to the HB3var3 variant recognized the surface of infected erythrocytes and abolished the binding of infected erythrocytes to brain endothelial cells. The subset of Group A PfEMP1 variants identified here provides a new target for interventions to treat or prevent cerebral malaria.
2011-11-01 | GSE32211 | GEO
Project description:PBMCs were obtain from mild malaria and cerebral malaria patient at the onset of P. falciparum infection. Patient recruitment took place in two hospital centers in Senegal Total RNAs from PBMCs of mild and cerebral malaria patients were profiled after hybridization with Agilent SurePrint G3 Human GE 8x60K Microarray to identify blood biomarkers for cerebral malaria phenotype Plasmodium falciparum malaria remains a major health problem in Africa. The mechanisms of pathogenesis leading to the severe form of the disease are not fully understood. Blood transcriptional profiles were investigated in patient with cerebral malaria, noncerebral malaria , and mild malaria by using the microarray technology. We identified a set of 447 genes that was differentially expressed between the three patient groups after a false discovery rate of 10%. Since the cerebral patients displayed a particular transcriptional pattern, we focused our analysis on the differences between cerebral malaria patients and mild malaria patients. We further found 849 genes differentially expressed after a false discovery rate of 10%. We validated our results by using the qPCR method for 5 genes. The enrichment analysis of their functional annotation indicates that genes involved in A, B, C pathways play a role in the occurrence of cerebral malaria. These results provide new insight into the potential effect of the dysregulation of gene expression and specific pathways. Host genetic variation may partly explain such alteration of gene expression. Further studies are required to investigate this in African populations.
2019-10-07 | GSE116306 | GEO