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Title: New generation lipid emulsion protects against LPS-induced brain inflammation in pemature piglets

Author
item GUTHRIE, GREGORY - Children'S Nutrition Research Center (CNRC)
item HODGES, BENJAMIN - Children'S Nutrition Research Center (CNRC)
item MARTIN, CAMILIA - Harvard Medical School
item STOLL, BARBARA - Children'S Nutrition Research Center (CNRC)
item OLUTOYE, OLUYINKA - Texas Children'S Hospital
item FREEDMAN, STEVEN - Harvard Medical School
item Burrin, Douglas - Doug

Submitted to: Archives of Disease in Childhood
Publication Type: Abstract Only
Publication Acceptance Date: 7/29/2014
Publication Date: 10/17/2014
Citation: Guthrie, G., Hodges, B., Martin, C.R., Stoll, B., Olutoye, O.O., Freedman, S.D., Burrin, D.G. 2014. New generation lipid emulsion protects against LPS-induced brain inflammation in pemature piglets. Archives of Disease in Childhood. 99(Suppl 2):PS-341a, A235.

Interpretive Summary:

Technical Abstract: 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. The aim is 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). 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, subgroups 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 indicated that 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 antiinflammatory 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. In conclusions, SMOFlipid protected against LPS-induced inflammation, but did not acutely increase the expression of the neuroprotective protein, BDNF, in the presence of LPS.