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Lipid-enriched and protein-enriched enteral nutrition limits inflammation in a human endotoxemia model

Introduction

Enteral administration of lipid-enriched nutrition was previously shown to attenuate inflammation and organ damage via a cholecystokinin-mediated vagovagal reflex in animal studies. The current proof-of-principle study investigates the immunomodulatory potential of enteral lipid-enriched and protein-enriched nutrition during experimental human endotoxemia.

Methods

After an overnight fast, 18 healthy male subjects received an intravenous bolus of Escherichia coli lipopolysaccharide (LPS; 2 ng/kg). Subjects in the fasted group (n = 6) were deprived of food throughout the study, while subjects in the intervention groups were fed either enriched (n = 6) or isocaloric control nutrition (n = 6) via a nasojejunal tube, starting 1 hour prior to LPS administration until 6 hours afterwards.

Results

LPS administration resulted in a marked inflammatory response. Continuous postpyloric administration of nutrition increased plasma cholecystokinin levels. Enriched nutrition attenuated circulating levels of the proinflammatory cytokines TNFα and IL-6 and the IL-1 receptor antagonist compared with control nutrition (all: P < 0.01) and fasted subjects (all: P < 0.05). Additionally, enriched nutrition augmented the anti-inflammatory response, reflected by increased IL-10 release compared with fasted subjects (P < 0.0001). See Figure 1.

Figure 1
figure 1

Plasma cytokine levels in the three experimental groups.

Conclusions

The current study establishes the anti-inflammatory potential of enriched nutrition in humans. The immediate anti-inflammatory effect of enriched nutrition suggests that the beneficial effects are mediated via a cholecystokinin-dependent vagovagal reflex. Enteral administration of enriched nutrition is a promising intervention to modulate the immune response in the early course of systemic inflammation.

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Kox, M., Lubbers, T., De Haan, J. et al. Lipid-enriched and protein-enriched enteral nutrition limits inflammation in a human endotoxemia model. Crit Care 15 (Suppl 1), P383 (2011). https://doi.org/10.1186/cc9803

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