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Background    Toxoplasma gondii , a common opportunistic protozoan, is a leading cause of illness and mortality among immunosuppressed individuals and during congenital infections. Current therapeutic strategies for toxoplasmosis are not fully effective at curtailing disease progression in these cases. Given the parasite ability to influence host immunity and metabolism, understanding of the metabolic alterations in the host’s immune organs during  T. gondii  infection may enhance the understanding of the molecular mechanisms that define the pathophysiology of  T. gondii  infection.    Methods  We investigated the global metabolic changes in the spleen of BALB/c mice at early and late stage of infection with  T. gondii  using LC-MS/MS-based metabolomics. Multivariate data analysis methods, principal components analysis (PCA) and partial least squares discriminant analysis (PLS-DA), were used to identify metabolites that are influenced by  T. gondii  infection.    Results  Multivariate analyses clearly separated the metabolites of spleen of infected and control mice. A total of 132 differential metabolites were identified, 23 metabolites from acutely infected  versus  control mice and 109 metabolites from chronically infected  versus  control mice. Lipids, hormones, lactones, acids, peptides, antibiotics, alkaloids and natural toxins were the most influenced chemical groups. There were 12 shared differential metabolites between acutely infected  versus  control mice and chronically infected  versus  control mice, of which 4,4-Dimethyl-5alpha-cholesta-8,14,24-trien-3beta-ol was significantly upregulated and ubiquinone-8 was significantly downregulated. Major perturbed metabolic pathways included primary bile acid biosynthesis, steroid hormone biosynthesis, biotin metabolism, and steroid biosynthesis, with arachidonic acid metabolism being the most significantly impacted pathway. These metabolic changes suggest a multifactorial nature of the immunometabolic responses of mouse spleen to  T. gondii  infection.    Conclusions  This study demonstrated that  T. gondii  infection can cause significant metabolomic alterations in the spleen of infected mice. These findings provide new insights into the molecular mechanisms that underpin the pathogenesis of  T. gondii  infection.    Electronic supplementary material  The online version of this article (doi:10.1186/s13071-017-2282-6) contains supplementary material, which is available to authorized users.

Profiling of the perturbed metabolomic state of mouse spleen during acute and chronic toxoplasmosis