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  • Open Access

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

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Critical Care201115 (Suppl 1) :P383

  • Published:


  • Cholecystokinin
  • Fast Subject
  • Fast Group
  • Immunomodulatory Potential
  • Enteral Administration


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.


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.


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.


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.

Authors’ Affiliations

Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands
Maastricht University Medical Centre, Maastricht, the Netherlands
Atrium Medical Center, Heerlen, the Netherlands


© Kox et al. 2011

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.