Glutamine-enriched enteral nutrition increases in vitro interferon-gamma production but does not influence the in vivo specific antibody response to KLH after severe trauma. A prospective, double blind, randomized clinical study

Abstract

Background & aims: Severe trauma leads to an immune suppression, characterized by a Type 2 T-lymphocyte response, contributing to the susceptibility of infectious complications. Plasma concentrations of glutamine (GLN), the preferred fuel for immunocompetent cells, severely decrease after trauma. Since administering glutamine-enriched enteral nutrition (EN) reduces infectious complications in trauma patients, we compared the effect of glutamine-enriched EN with an isocaloric, isonitrogenous enteral control (Con) feeding, on the Type 1 and 2 T-lymphocyte responses.

Methods: Thirty-eight trauma patients (Injury Severity Score >20) were sensitized with Keyhole Limpet Hemocyanin (KLH) within 12 h after trauma (17 GLN group). Healthy volunteers served as controls (HV, n=17). In vitro interferon-gamma (IFN-gamma), IL-4 and IL-10 productions of phytohemagglutinin (PHA)-stimulated PBMCs were determined by ELISA technique. KLH-specific IgG, IgM, IgA, IgG1, IgG2, IgG3, IgG4 and IgE were measured in serum.

Results: Both patient groups had a low in vitro (IFN-) production of stimulated PBMCs on d1. On d14, the IFN-gamma production increased significantly in the glutamine group as compared to the controls. IL-4 production was not different between the groups on day 1 (d1). On d14, IL-4 decreased in the control group as compared to the glutamine group. KLH-specific antibodies reached comparable levels in both patients groups and healthy volunteers at d14.

Conclusions: In conclusion, trauma caused a suppressed in vitro cellular immune response presented by a low IFN-gamma production and depressed the IgG and IgM response to KLH directly after trauma. Glutamine increased IFN-gamma production (d14), maintained a normal IL-4 production, but was not acquired for the development of KLH-specific humoral response on d14, in sync suggesting that dietary glutamine supports the restoration of the Type-1 T-lymphocyte responsiveness.