Whole genome expression array of malaria infected human hosts
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE116149 | GEO | 2018/06/23
REPOSITORIES: GEO
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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:Whole genome expression array of malaria infected human hosts
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2018-10-26 | PXD005048 | Pride
Project description:Plasmodium falciparum, a lethal protozoan, undergoes a complex extra- and intraerythrocytic development cycle that requires intricate and flexible regulatory mechanisms in order to facilitate reproduction and maintain the parasite’s resistance to environmental stress. Protein post-translational modifications (PTMs) are essential processes following protein biogenesis that allow proteins to fulfill their diverse biological functions. Here, we present comprehensive PTMomic profiling of both P. falciparum and its erythrocytic host cells during the 48 hours after infection. Fine mappings of each protein in both P. falciparum and the infected red blood cells (pRBCs) were accomplished. More than two-thirds of the parasite and its host cell proteins underwent extensive and dynamic modification throughout the erythrocytic developmental stage of the malarial parasite. Apart from the finding that PTMs actively regulated P. falciparum gene activation and silencing, the key molecules involved in the host-parasite interaction and pathogenesis were essentially modified. The establishment of an atlas of PTMomes of P. falciparum and its host erythrocytes will promote a deeper understanding of the parasite biology and will provide a basis for the search for novel antimalarials.
2020-11-09 | PXD017503 | 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:After entering their mammalian host via the bite of an Anopheles mosquito, Plasmodium sporozoites migrate to the liver where they traverse several hepatocytes before invading the one inside which they will develop and multiply into thousands of merozoites. Although this constitutes an essential step in malaria infection, the requirements of Plasmodium parasites in liver cells and how they use the host cell for their own survival and development are poorly understood. To gain new insights into the molecular host-parasite interactions that take place during malaria liver infection, we have used high-throughput microarray technology to determine the transcriptional profile of P. yoelii-infected hepatocytes that were collected from P. yoelii-infected mice 24 and 40 h after infection. This in vivo microarray expression was compared with the microarray analysis of in vitro infected hepatoma cells infected with closely related rodent malaria parasite P. berghei. Differential expression patterns for host genes identify genes and pathways involved in the host response to rodent Plasmodium parasites. Keywords: gene expression
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2016-09-01 | GSE72049 | GEO
Project description:Purpose: this study is to analyze the change of overall transctiption after disruption of Protein Arginine Methyltranferase 5 (PRMT5) in Plasmodium falciparum. Methods: In this study, the transcriptomes of a PfPRMT5 gene knockout (KO) parasite line with its wildtype control were analyzed a custom-desinged Agilent microarray.Total RNA were harvested from the asexual parasites at four stages (ring, early trophozoite, late trophozoite, and schizont)(12h, 24h, 36h, and 46h post-invasion) using the Quick-RNA MiniPrep kit (Zymo Research).
2023-06-28 | GSE199419 | GEO
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>
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2016-02-15 | E-GEOD-35860 | biostudies-arrayexpress