Abstract
BackgroundThe protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.MethodsWe have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.ResultsOur results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), l-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, l-homophenylalanine, oleic acid and ceramide (d18:1/16:0).ConclusionsOur data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.
Highlights
The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals
Animal infection and cerebral cortex collection Mice were infected with T. gondii PRU strain to produce tissue cysts that were subsequently used for the infection experiments
The mice in infected groups were challenged by oral gavage with 10 cysts of T. gondii PRU strain suspended in 0.5 ml phosphatebuffered saline (PBS), whereas mice in the control groups were mock-treated with an equal volume of PBS only
Summary
The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. Toxoplasma gondii has an indirect, multistage life-cycle that involves tachyzoites, bradyzoites-containing cysts and oocysts. This parasite has an exceptionally wide range of intermediate hosts including almost all warm-blooded vertebrate animals and humans. Tachyzoites and bradyzoites occur in the tissues of the intermediate hosts. Members of the family Felidae are the only animals that can serve as the definitive host of T. gondii, where gametogony occurs in their intestine, resulting in the formation and excretion of oocysts in the feces. Ingestion of infectious oocysts with contaminated food or water, or eating improperly cooked or raw meat containing tissue cysts are the two main routes of T. gondii infection in humans
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