Summary of project PR002700

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002700. The data can be accessed directly via it's Project DOI: 10.21228/M8NK11 This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR002700
Project DOI:doi: 10.21228/M8NK11
Project Title:Loss of vitamin C biosynthesis protects from the pathology of a Schistosome infection
Project Type:MS quantitative analysis
Project Summary:Schistosoma parasite is known to require ascorbate to produce eggs in vitro culture. To investigate the effect of ascorbate deficiency in mice infected with Schistosoma mansoni, the pathology of infection was analyzed in vivo. S. mansoni required host ascorbate to produce eggs and consequently, ascorbate-deficient mice were protected from schistosomiasis pathologies including liver granuloma formation and transmission. To understand the processes dependent on ascorbate metabolome and gene expression profiles were compared between Ascorbate-treated and -untreated samples. Our work shows that ascorbate deficiency can have physiological benefits by protecting animals from the pathology of a major parasitic disease.
Institute:UT Southwestern Medical Center
Department:CRI
Laboratory:Michalis Agathokleous
Last Name:Agathokleous
First Name:Michalis
Address:5323 Harry Hines Blvd, Children's Research Institute, Dallas, TX, 75309, USA
Email:michail.agathokleous@utsouthwestern.edu
Phone:2146486270

Summary of all studies in project PR002700

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)
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(* : Contains raw data)
ST004274 Loss of vitamin C biosynthesis protects from the pathology of a Schistosome infection and egg production. Schistosoma mansoni University of Texas Southwestern Medical Center at Dallas MS 2025-10-31 1 10 Uploaded data (1.7G)*
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