Untargeted Lipidomics Reveals Lipid Alterations in Colonic Contents of C57BL/6J Mice with Acute Toxoplasma gondii Infection
TL;DR
The findings provide a novel metabolic perspective on the intestinal pathogenesis of toxoplasmosis and offer exploratory candidate lipid markers for diagnosing acute infection.
Abstract
Background: Although Toxoplasma gondii has been recognized as an obligate intracellular parasite, the lipid metabolic alterations it induces in colonic contents during acute infection remain poorly characterized. Methods: An acute infection model was established using C57BL/6J mice by oral inoculation with the T. gondii ME49 strain. Untargeted lipidomics analysis was performed on the colonic contents collected at day 10 post-infection. Results: Acute infection significantly elevated glycerophospholipids (GPs) and reduced glycerolipids (GLs), and prenol lipids (PRs), leading to 136 differentially abundant lipids. Pathway enrichment analysis identified the two most significantly affected pathways: choline metabolism in cancer and glycerophospholipid metabolism, with lysophosphatidic acid (LPA(16:0)) and lysophosphatidylcholine (LPC(18:1)) functioning as core hub nodes. Receiver operating characteristic (ROC) analysis identified phosphatidylethanolamine (PE(20:1e_22:4)), PE(16:0_22:6), hexosylceramide (Hex1Cer(m18:0_20:4)), and Hex1Cer(t17:0_22:6) as exploratory candidate biomarkers with high discriminatory performance (AUC > 0.94). Conclusions: Acute T. gondii infection induces lipid metabolic reprogramming in colonic contents of C57BL/6J mice. The findings provide a novel metabolic perspective on the intestinal pathogenesis of toxoplasmosis and offer exploratory candidate lipid markers for diagnosing acute infection.