Rapid cerebral metabolic shift during neonatal sepsis is attenuated by enteral colostrum supplementation in preterm pigs

Research output: Contribution to journalJournal articleResearchpeer-review

Masoumeh Alinaghi, Ping Ping Jiang, Anders Brunse, Per Torp Sangild, Hanne Christine Bertram

Sepsis, the clinical manifestation of serious infection, may disturb normal brain development, especially in preterm infants with an immature brain. We hypothesized that neonatal sepsis induces systemic metabolic alterations that rapidly affect metabolic signatures in immature brain and cerebrospinal fluid (CSF). Cesarean-delivered preterm pigs systemically received 10 9 CFU/kg Staphylococcus epidermidis (SE) and were provided total parenteral nutrition (n = 9) or enteral supplementation with bovine colostrum (n = 10) and compared with uninfected pigs receiving parenteral nutrition (n = 7). Plasma, CSF, and brain tissue samples were collected after 24 h and analyzed by 1 H NMR-based metabolomics. Both plasma and CSF metabolomes revealed SE-induced changes in metabolite levels that reflected a modified energy metabolism. Hence, increased plasma lactate, alanine, and succinate levels, as well as CSF lactate levels, were observed during SE infection (all p < 0.05, ANOVA analysis). Myo-inositol, a glucose derivative known for beneficial effects on lung maturation in preterm infants, was also increased in plasma and CSF following SE infection. Enteral colostrum supplementation attenuated the lactate accumulation in blood and CSF. Bloodstream infection in preterm newborns was found to induce a rapid metabolic shift in both plasma and CSF, which was modulated by colostrum feeding.

Original languageEnglish
Article number13
JournalMetabolites
Volume9
Issue number1
Number of pages15
ISSN2218-1989
DOIs
Publication statusPublished - 2019

    Research areas

  • Bioactive dairy components, Bloodstream infection, Brain metabolites, Cerebral metabolism, Cerebrospinal fluid, Enteral feeding, Neonatal sepsis, NMR metabolomics, Preterm infants, Staphylococcus epidermidis

Number of downloads are based on statistics from Google Scholar and www.ku.dk


No data available

ID: 217112042