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Review
. 2009 Jan;394(1):17-30.
doi: 10.1007/s00423-008-0339-x. Epub 2008 Jun 3.

Food fight! Parenteral nutrition, enteral stimulation and gut-derived mucosal immunity

Affiliations
Review

Food fight! Parenteral nutrition, enteral stimulation and gut-derived mucosal immunity

Joshua L Hermsen et al. Langenbecks Arch Surg. 2009 Jan.

Abstract

Introduction: Nutrition support is an integral component of modern patient care. Type and route of nutritional support impacts clinical infectious outcomes in critically injured patients.

Discussion: This article reviews the relationships between type and route of nutrition and gut-derived mucosal immunity in both the clinical and laboratory settings.

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Figures

Figure 1
Figure 1
Schematic representation of a typical mucosal immune response. The process begins with antigen sampling and recognition at inductive sites and ends with the generation of antigen specific secretory immunoglobulin A at effector sites which is actively transported to the mucosal surface.
Figure 2
Figure 2
The relationship between pIgR and dimeric IgA. Dimeric IgA generated in the lamina propria is bound, and transported across the epithelium, by pIgR. As the pIgR/IgA complex is released into the lumen, a portion of the pIgR protein remains with the IgA to form secretory IgA. Free secretory component is generated if pIgR is transported without first binding IgA.
Figure 3
Figure 3
The level of MAdCAM-1 and the numbers of lymphocytes in the Peyer’s patches decline in parallel fashion with parenteral feeding / decreased enteral stimulation. These changes are reversed with refeeding of an enteral diet.
Figure 4
Figure 4
The level of pIgR in the small intestine declines in a stepwise fashion according to type and route of nutrition. CED= complex enteral diet (ie: tube feeds), IG-PN= intragastric parenteral nutrition (ie: elemental diet), IV-PN= intravenous parenteral nutrition.
Figure 5
Figure 5
IgA levels in the intestinal and respiratory tracts decline with parenteral feeding / decreased enteral stimulation.
Figure 6
Figure 6
Injury causes acute increases in respiratory tract IgA levels in both humans and mice.
Figure 7
Figure 7
Injury induced increases in respiratory tract IgA are abrogated by pre-injury parenteral feeding / decreased enteral stimulation or pre-injury blockade of tumor necrosis factor alpha function with a monoclonal antibody.

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