Abstract
Eimeria bovis is an intracellular apicomplexan parasite that causes considerable economic losses in the cattle industry worldwide. During the first merogony, E. bovis forms large macromeronts with >140,000 merozoites I in host endothelial cells. Because this is a high-energy demanding process, E. bovis exploits the host cellular metabolism to fulfill its metabolic requirements. We here analyzed the carbohydrate-related energetic metabolism of E. bovis–infected primary bovine umbilical vein endothelial cells during first merogony and showed that during the infection, E. bovis–infected culture presented considerable changes in metabolic signatures, glycolytic, and mitochondrial responses. Thus, an increase in both oxygen consumption rates (OCR) and extracellular acidification rates (ECAR) were found in E. bovis–infected host cells indicating a shift from quiescent to energetic cell status. Enhanced levels of glucose and pyruvate consumption in addition to increased lactate production, suggesting an important role of glycolysis in E. bovis–infected culture from 12 days p.i. onward. This was also tested by glycolytic inhibitors (2-DG) treatment, which reduced the macromeront development and diminished merozoite I production. As an interesting finding, we observed that 2-DG treatment boosted sporozoite egress. Referring to mitochondrial activities, intracellular ROS production was increased toward the end of merogony, and mitochondrial potential was enhanced from 12 d p. i. onward in E. bovis–infected culture. Besides, morphological alterations of membrane potential signals also indicated mitochondrial dysfunction in macromeront-carrying host endothelial culture.
Highlights
Eimeria bovis is an obligate intracellular parasite that belongs to the subphylum Apicomplexa
The purpose of the present work is to analyze the energetic metabolism of E. bovis–infected primary bovine host endothelial cells and to explore the respective status of premature senescence observed in this host cell type
E. bovis is an intracellular parasite that exclusively develops in bovine endothelial cells in vivo
Summary
Eimeria bovis is an obligate intracellular parasite that belongs to the subphylum Apicomplexa. E. bovis macromeront development takes approximately 24 days until merozoite type I production takes place (Hermosilla et al, 2002) and increased demand of energy and cell building blocks for phospholipids, cholesterol, nucleic acids, amino acids, proteins, and organelles (Taubert et al, 2010; Hermosilla et al, 2012). Former transcriptomic analyses of E. bovis–infected host endothelial cells indicated an impact of this obligate intracellular parasite on host cellular carbohydrate, amino acid, and folic acid metabolism, as well as energy production because several enzymes, such as galactose-1phosphate uridylyltransferase, UDP-glucose glycoprotein glucosyltransferase 2, methylene-tetrahydrofolatedehydrogenase, malic enzyme 1, or malate dehydrogenase 1, were found significantly up-regulated at 14 days post infection A sub-set of up-regulated genes in E. bovis–infected host cells revealed to be involved in carbohydrate synthesis and metabolism, such as amino sugar, fructose/mannose, galactose, nucleotide sugar, and pyruvate metabolism, as well as in glycolysis/gluconeogenesis and the pentose phosphate pathway (Taubert et al, 2010). T. gondii and P. falciparum rely on the prokaryotic type II fatty acid synthesis pathway (FASII) (Waller et al, 1998)
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