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Background: During sepsis pro-inflammatoric cytokines like TNFα are released from the gut leading to multiorgan dysfunction. An enteral diet in form of lipid is able to reduce intestinal inflammation during sepsis via the “cholinergic anti-inflammatory pathway”. The anti-inflammatory cytokine IL10, mainly produced in the liver, is important in the control of inflammation.Aim: To investigate the role of enteral omega-9 fatty acid based immunonutrition in from of olive oil during sepsis on hepatic IL10 expression. Methods: Mesenteric lymph was obtained from lymph fistula donor rats during sepsis (lipopolysaccharides [LPS], 5 mg/kg i.p.) with or without enteral immunonutrition (2% olive oil or isocaloric control solution). Lymph was collected in two hours intervals and the TNFα and IL10 release from the gut was measured with ELISA. Liver tissue was harvested after 3 and 6 hours and liver damage was quantified by TUNEL-immunoreactivity. Intrahepatic IL10 was measured by Western Blot. Results: During sepsis TNFα is released in high concentration into mesenteric lymph, peaking at 2h. Immunonutrition containing ω-9 fatty acids is able to reduce TNFα-release during sepsis (control vs. ω-9 fatty acids ; pg/ml; basal: 45±12 vs. 32±15; 1-2h: 10683±1402 vs. 2330±1279*; 3-4h: 4784±2145 vs. 897±662; 5-6h: 105±27 vs. 75±26; *p<0,05). The maximal IL10 release is clearly after the peak of TNFα, being interestingly 2 times lower in the group obtaining immunonutrition. Concentration of hepatic IL10 was 77% lower during olive oil based nutrition and the number of apoptotic hepatic cells during sepsis was significantly lower in the group receiving enteral immunonutrition (TUNEL-pos. cells; control: 25±5; ω-9 fatty acids: 9±1 p<0,05).Conclusions: A ω-9 fatty acid based enteral nutrition reduces the inflammation in the gut and has an hepatoprotective effect during sepsis. The IL10 release is proportional to the inflammation. The anti-inflammatory effect of ω-9 fatty acids is not due high LI10 expression. IL10 release is likely to be reactive to inflammation and its expression is probably secondary to inflammation.