Plasmodium falciparum hrp2 deletion
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ABSTRACT:
PROVIDER: PRJEB44806 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human cerebral malaria (HCM) is a severe complication of Plasmodium falciparum infection associated with high mortality rates predominantly in children that live in sub-Saharan Africa. Histine rich protein 2 (HRP2) is a diagnostic and prognostic marker that can be detected in peripheral blood, cerebrospinal fluid and cord blood. Recent studies confirm that HRP2 crossess the compromised blood brain barrier (BBB) during HCM and infiltrate brain parenchyma. Treatments with HRP2 in murine experimental cerebral malaria (ECM) model recapitulate these effects. We tested the hypothesis that treatment of induced pluripotent stem cells (iPSC)-derived brain cortical organoids with HRP2 will recapitulate the brain effects. We assessed the effects of HRP2 treatment on ultrastructure, expression of markers of viability and inflammation neurons, astrocytes and microglia in organoids. We tested the neuroprotective effects of Neuregulin 1 (NRG1) against the HRP2 treatment. In the study presented here, we assessed the inflammatory genes induced by HRP2 using the Immunology Panel on the nCounter system (NanoString) and results were analyzed using nSolver softaware.
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2026-07-21 | E-MTAB-14868 | biostudies-arrayexpress
Project description:Human cerebral malaria (HCM) is a severe complication of Plasmodium falciparum (P.f.) infection that is characterized by capillary occlusions, rupture of the blood-brain barrier (BBB) and perivascular cellular injury. P.f. histidine-rich protein 2 (HRP2), a byproduct of parasitized red blood cell (pRBC) lysis, crosses the BBB when compromised to cause brain injury. We hypothesized that HRP2-induced neuronal damage can be attenuated by Neuregulin 1 (NRG1), an anti-inflammatory neuroprotective factor. Using brain cortical organoids, we determined that HRP2 upregulated cell death and inflammatory markers and disorganized brain organoid tissue. We identified Toll Like Receptors (TLR1 and 2) as potential mediators of HRP2-induced cellular damage and inflammation. Exogenous treatment of organoids with NRG1 attenuated HRP2 effects. The results indicate that HRP2 mediates malaria-associated HRP2-induced brain injury and inflammation and that NRG1 may be an effective therapy against HRP2 effects in the brain. In the study presented here, we assessed the inflammatory genes induced by HRP2 using the Immunology Panel on the nCounter system (NanoString) and results were analyzed using nSolver softaware.
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Project description:Malaria is a major global health threat, with millions of cases and hundreds of thousands of deaths reported annually, primarily in sub-Saharan Africa. Children under five years of age residing in holoendemic Plasmodium falciparum transmission regions are the most vulnerable to malaria, accounting for vast majority of cases and mortality. The major clinical manifestation of severe malaria in these children is severe malarial anemia [SMA, hemoglobin (Hb)<6.0 g/dL]. The molecular mechanisms underlying SMA pathogenesis, particularly the contribution to this disease process of P. falciparum gene activities at transcriptomic levels, remain largely unexplored. As such, the overall objective of the study was to profile the blood-stage Plasmodium falciparum transcriptome in children with SMA. To achieve this goal, we performed RNAseq on total RNA from peripheral blood samples of 60 pediatric malaria patients (3-36 months) with non-SMA (Hb≥6.0 g/dL, n=40) and SMA (n=20) at enrollment. The RNA reads were mapped to the P. falciparum reference genome (PfKE01). Diffentially expressed genes (DEGs) in SMA relative to non-SMA and relevant biological pathways in P. falciparum were identified. In addition, the performance of the expressed parasite genes in predicting SMA was assesed. These findings promote the identification of potential parasite-derived biomarkers and therapeutic targets for improving SMA management.
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