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PS-341a New Generation Lipid Emulsion Protects Against Lps-induced Brain Inflammation In Premature Piglets
  1. G Guthrie1,
  2. B Hodges1,
  3. C Martin2,
  4. B Stoll1,
  5. O Olutoye3,
  6. S Freedman4,
  7. D Burrin1
  1. 1Pediatrics, USDA/ARS Children’s Nutrition Research Center/Baylor College of Medicine, Houston, USA
  2. 2Neonatology, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, USA
  3. 3Surgery, Texas Children’s Hospital, Houston, USA
  4. 4Medicine, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, USA

Abstract

Background Premature infants provided parenteral nutrition (PN) high in n-6 polyunsaturated fatty acids (PUFA) have increased risk of inflammatory disease, such as nosocomial sepsis. The pro-inflammatory insult can also contribute to injury and delayed neuronal growth in the perinatal brain. Provision of high long chain n-3 PUFA in parenteral lipids is associated with decreased inflammation and incidence of sepsis. The provision of n-3 PUFA, especially docosahexaenoic acid (DHA) also is critical for neurodevelopment in premature infants.

Aim To determine whether a new generation lipid emulsion high in n-3 PUFA (SMOFlipid) protects against inflammation and improves neuroprotection in response to lipopolysaccharide (LPS) compared to a lipid emulsion high in n-6 PUFA (Intralipid).

Methods Preterm piglets delivered 7 d preterm were assigned into two groups receiving complete TPN containing either Intralipid or SMOFlipid at 10 g*kg-1*d-1 for 10 d. On day 10, sub-groups of piglets were assigned to receive either an 8-hr infusion of lipopolysaccharide (2 mg/kg) or control saline and target gene expression in brain tissue was analysed.

Results LPS increased brain gene expression of pro-inflammatory cytokines IL-6, IL-8, and TNF in the Intralipid group, but not the SMOFlipid group. The gene expression of the anti-inflammatory cytokine Il-10 was increased in both LPS-treated lipid groups. Brain-derived neuronal growth factor, a marker of neuronal proliferation, was deceased in the LPS-treated SMOFlipid group, but not the LPS-treated Intralipid group.

Conclusions SMOFlipid protected against LPS-induced inflammation, but did not acutely increase the expression of the neuroprotective protein, BDNF, in the presence of LPS.

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