Summary of Study ST002698

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001670. The data can be accessed directly via it's Project DOI: 10.21228/M8V14H This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002698
Study TitleSystemic host inflammation induces stage-specific transcriptomic modification and slower maturation in malaria parasites
Study TypeBiomedical research
Study SummaryWe found that host inflammation altered the plasma environment surrounding Plasmodium falciparum parasites in vivo, and that this altered plasma environment contained inhibitory factors that directly impaired maturation of early trophozoite stages. We demonstrated with LPS-conditioning that systemic host inflammation alone, in the absence of confounding factors such as ongoing infection, slowed the rate at which parasites transited from one generation of RBC to the next. While this is consistent with the idea that host inflammatory responses can impair parasite maturation, other TLR agonists, CpG and Poly I:C, did not elicit such a response. Metabolomics also identified 1-methylhypoxanthine as elevated in both LPS conditioned and acutely-infected plasma. Plasmodium survival depends on host hypoxanthine, inosine and xanthine for purine synthesis. 1-Methylhypoxanthine can bind effectively to and possibly limit the action of hypoxanthine-guanine phosphoribosyl transferase (HGPRTase)25, an enzyme critical for purine synthesis. Interestingly, hypoxanthine, inosine and xanthine were also all reduced in the plasma of LPS-conditioned and acutely infected mice supporting the possibility that inhibition of purine synthesis by 1-methylhypoxanthine might have been partly aided by the lack of substrates for this pathway.
Peter Doherty Institute for Infection and Immunity
DepartmentDepartment of Microbiology and Immunology
LaboratoryAshraful Haque lab
Last NameSkinner
First NameOliver
Address792 Elizabeth Street, The University of Melbourne, Victoria 3000 Australia
Phone+61 424088268
Submit Date2023-04-29
Num Groups5
Total Subjects25
Num MalesNA
Num FemalesNA
Study CommentsMalaria parasite cultures treatments: CpG, LPS, PbA, PIC, Saline
PublicationsSystemic host inflammation induces stage-specific transcriptomic modification and slower maturation in malaria parasites
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2023-06-26
Release Version1
Oliver Skinner Oliver Skinner application/zip

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Collection ID:CO002794
Collection Summary:C57BL/6J mice were purchased from the Animal Resource Centre (Perth, Australia). C57BL/6J.rag1−/− mice were bred at QIMR Berghofer Medical Research Institute. All mice were female between 6-12 weeks of age and were maintained under conventional conditions. Plasmodium berghei ANKA parasites constitutively expressing high-levels of eGFP (for RBC adoptive transfer), or luciferase (for establishing acute infection, although bioluminescence was not utilised), were sourced and used as previously reported12,16,17. PbA parasites were used after defrosting cryopreserved infected blood and a single in vivo passage in C57BL/6J mice. RBCs were collected from passage mice by cardiac puncture and used to infect with 105 pRBCs via lateral tail vein injection.
Sample Type:infected Red Blood Cells
Storage Conditions:-80℃