Transcript data from a severe malaria study
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE289197 | GEO | 2025/03/25
REPOSITORIES: GEO
Similar Datasets
Project description:Metabolome data from cerebral malaria cases and uncomplicated malaria controls in a case-control study in Mali.
2025-01-22 | MSV000096913 | MassIVE
Project description:Proteome data from cerebral malaria cases and uncomplicated malaria controls in a case-control study in Mali.
2025-03-25 | PXD058621 | Pride
Project description:We aimed at finding differently expressed genes in whole blood cells of African children with asymptomatic Plasmodium falciparum infection (A), uncomplicated malaria (U), severe malarial anemia (A) and cerebral malaria (Ce) compared one to another and to healthy children (Co). Understanding malarial immunopathology in the human host represents and enormous challenge for transcriptomic research. In this work, we used microarray and real-time RT-PCR technology to pursue deeper knowledge about the mechanisms underlying this disease in African children. To this end, we investigated the genomic transcriptional profiles in whole blood of healthy children and children with asymptomatic infection, uncomplicated malaria, malaria associated with severe anemia and cerebral malaria and compared them with previously published microarray results. We were able to discriminate between the different presentations of P. falciparum infection using supervised and unsupervised clustering of microarray data and unsupervised double-hierarchical clustering of real-time RT-PCR results of a set of 22 genes known to be expressed in at least one of the principal blood cell lineages. We further found considerable overlap between genes regulated in Kenyan and Gabonese children with symptomatic malaria, in contrast to adults with acute malaria from Cameroon. Different signatures for transcription factor binding sites in promoters of genes either up-regulated in symptomatic disease, specifically up-regulated in uncomplicated malaria or specifically down-regulated in cerebral malaria point out that similar gene expression in each of these clinical presentations is probably a result of common regulation at the transcriptional level. Immunoglobulin production, complement regulation and IFN beta signalling emerged as most discrepant features between uncomplicated malaria and all other investigated presentations, correlating with IRF7 and ISRE binding signatures in the corresponding genes. Down-regulation of several genes in cerebral malaria seems instead to be a response to hypoxia orchestrated by AhRF, GABP and HIF1 transcription factors. ARG1, BPI, CD163, IFI27, HP and TNFAIP6 transcript levels correlated positively with lactatemia and inversely with hemoglobin concentration and should be evaluated as prognostic markers to direct early therapeutic measures and prevent malarial disease evolution and death.
2019-01-23 | GSE1124 | GEO
Project description:Genome wide transcriptome analyses could reveal whether parasites causing severe malarial disease express different genes to those causing uncomplicated malaria. This knowledge could inform therapy and vaccine design targeting severe disease. Venous samples were collected from patients with severe (n=23) and uncomplicated (n=21) malaria attending a healthcare facility in Timika, Papua Province, Indonesia. This area has unstable malaria transmission with estimated annual parasite incidence of 450 per 1000 population and symptomatic illness in all ages. Severe malaria was defined as peripheral parasitaemia with at least one modified World Health Organization (WHO) criterion of severity. Erythrocytes were immediately isolated from whole blood, solubilised in RNA preservative and frozen. Libraries were 100 bp paired end sequenced on a 2500-HT Hiseq (Illumina) using RapidRun chemistry (Illumina).
2018-02-08 | E-MTAB-5860 | biostudies-arrayexpress
Project description:<p>Malaria varies in severity, with complications ranging from uncomplicated to severe malaria. Severe malaria could be attributed to peripheral hyperparasitemia or cerebral malaria. The metabolic interactions between the host and <em>Plasmodium</em> species are yet to be understood during these infections of varied pathology and severity. An untargeted metabolomics approach utilizing the liquid chromatography-mass spectrometry platform has been used to identify the affected host metabolic pathways and associated metabolites in the serum of murine malaria models with uncomplicated malaria, hyperparasitemia and experimental cerebral malaria. We report that mice with malaria share similar metabolic attributes like higher levels of bile acids, bile pigments, and steroid hormones that have been reported for human malaria infections. Moreover, in severe malaria, upregulated levels of metabolites like phenylalanine, histidine, valine, pipecolate, ornithine and pantothenate, with decreased levels of arginine and hippurate, were observed. Metabolites of sphingolipid metabolism were upregulated in experimental cerebral malaria. Higher levels of 20-hydroxy-leukotriene B4 and epoxyoctadecamonoenoic acids were found in uncomplicated malaria, with lower levels observed for experimental cerebral malaria. Our study provides insights into host biology during different pathological stages of malaria disease and would be useful for the selection of animal models for evaluating diagnostic and therapeutic interventions against malaria.</p>
2022-09-14 | MTBLS4387 | MetaboLights
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:Management of severe malaria remains a critical global challenge. In this study, using a multiplexed quantitative proteomics pipeline we systematically investigated the plasma proteome alterations in non-severe and severe malaria patients. We identified a few parasite proteins in severe malaria patients, which could be promising from a diagnostic perspective. Further, from host proteome analysis we observed substantial modulations in many crucial physiological pathways, including lipid metabolism, cytokine signaling, complement, and coagulation cascades in severe malaria. We propose that severe manifestations of malaria are possibly underpinned by modulations of the host physiology and defense machinery, which is evidently reflected in the plasma proteome alterations. Importantly, we identified multiple blood markers that can effectively define different complications of severe falciparum malaria, including cerebral syndromes and severe anemia. The ability of our identified blood markers to distinguish different severe complications of malaria may aid in developing new clinical tests for monitoring malaria severity.
2020-11-06 | PXD014991 | Pride
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
Project description:This study examined the differences in human and parasite gene expression pattern between children with severe malaria and those with uncomplicated malaria through a dual RNA-seq approach. Peripheral blood samples were collected which contained substantial numbers of parasites that required no RNA enrichment prior to library preparation and sequencing.
2018-06-20 | E-MTAB-6413 | biostudies-arrayexpress
Project description:<p>Malaria, caused by <em>Plasmodium</em> species, remains a significant cause of morbidity and mortality globally. Gut bacteria can influence the severity of malaria, but the contribution of specific bacteria to the risk of severe malaria is unknown. Here, multiomics approaches demonstrate specific species of <em>Bacteroides</em> are causally linked to the risk of severe malaria. <em>Plasmodium yoelii</em> hyperparasitemia-resistant mice gavaged with murine-isolated <em>Bacteroides fragilis</em> develop <em>P. yoelii</em> hyperparasitemia. Moreover, <em>Bacteroides</em> are significantly more abundant in Ugandan children with severe malarial anemia than with asymptomatic <em>P. falciparum</em> infection. Human isolates of <em>Bacteroides caccae</em>, <em>Bacteroides uniformis</em>, and <em>Bacteroides ovatus</em> but not <em>Bacteroides thetaiotaomicron</em> caused susceptibility to severe malaria in mice. However, the pathogenic potential of gut <em>Bacteroides</em> towards susceptibility to severe malaria is dependent on additional gut microbiota, indicating a consortium effect in severe malaria. Approaches that target gut <em>Bacteroides</em> may present an opportunity to prevent severe malaria and associated deaths.</p>
2023-09-13 | MTBLS3449 | MetaboLights