Microsporidia infection upregulates host energy metabolism but maintains ATP homeostasis.

摘要: Abstract Microsporidia are a group of obligate intracellular parasites which lack mitochondria and have highly reduced genomes. Therefore, they unable to produce ATP via the tricarboxylic acid (TCA) cycle oxidative phosphorylation. Instead, evolved strategies obtain manipulate host metabolism acquire nutrients. However, little is known about how microsporidia modulate energy metabolisms. Here, we present first targeted metabolomics study investigate changes in as result infection by microsporidian. Metabolites silkworm embryo cell (BmE) were measured 48 hours post Nosema bombycis. Thirty metabolites detected, nine upregulated mainly involved glycolysis (glucose 6-phosphate, fructose 1,6-bisphosphate) TCA (succinate, α-ketoglutarate, cis-aconitate, isocitrate, citrate, fumarate). Pathway enrichment analysis suggested that could promote synthesization nucleotides, fatty acids, amino acids host. concentration cells, however, was not significantly changed infection. This homeostasis also found Encephalitozoon hellem infected mouse macrophage RAW264.7, human monocytic leukemia THP-1, embryonic kidney 293, foreskin fibroblast cells. These findings suggest maintain levels while stimulating metabolic pathways provide additional nutrients for parasite.