title: Lack of effect of glutamine administration to boost the innate immune system response in trauma patients in the intensive care unit.
abstract: BACKGROUND
  The use of glutamine as a dietary supplement is associated with a reduced risk of infection. We hypothesized that the underlying mechanism could be an increase in the expression and/or functionality of Toll-like receptors (TLR), key receptors sensing infections. The objective of this study was to evaluate whether glutamine supplementation alters the expression and functionality of TLR2 and TLR4 in circulating monocytes of trauma patients admitted to the intensive care unit (ICU).
  
  
  METHODS
  We designed a prospective, randomized and single-blind study. Twenty-three patients received parenteral nutrition (TPN) with a daily glutamine supplement of 0.35 g/kg. The control group (20 patients) received an isocaloric-isonitrogenated TPN. Blood samples were extracted before treatment, at 6 and 14 days. Expression of TLR2 and TLR4 was determined by flow cytometry. Monocytes were stimulated with TLR specific agonists and cytokines were measured in cell culture supernatants. Phagocytic ability of monocytes was also determined.
  
  
  RESULTS
  Basal characteristics were similar in both groups. Monocytes from patients treated with glutamine expressed the same TLR2 levels as controls before treatment (4.9 ± 3.5 rmfi vs. 4.3 ± 1.9 rmfi, respectively; P = 0.9), at Day 6 (3.8 ± 2.3 rmfi vs. 4.0 ± 1.7 rmfi, respectively; P = 0.7) and at Day 14 (4.1 ± 2.1 rfim vs. 4.6 ± 1.9 rmfi, respectively; P = 0.08). TLR4 levels were not significantly different between the groups before treatment: (1.1 ± 1 rmfi vs 0.9 ± 0.1 rmfi respectively; P = 0.9), at Day 6 (1.1 ± 1 rmfi vs. 0.7 ± 0.4 rmfi respectively; P = 0.1) and at Day 14 (1.4 ± 1.9 rmfi vs. 1.0 ± 0.6 rmfi respectively; P = 0.8). No differences in cell responses to TLR agonists were found between groups. TLR functionality studied by phagocytosis did not vary between groups.
  
  
  CONCLUSIONS
  In trauma patients in the intensive care unit, TPN supplemented with glutamine does not improve the expression or the functionality of TLRs in peripheral blood monocytes.
  
  
  BACKGROUND
  ClinicalTrials.gov Identifier: NCT01250080.
authors.affiliation: Intensive Care Medicine Department, Son Dureta University Hospital, Andrea Doria 55, 07014, Palma de Mallorca, Spain. juan.perez@ssib.es
authors.forename: Jon
authors.initials: J
authors.lastname: Pérez-Bárcena
authors.forename: Catalina
authors.initials: C
authors.lastname: Crespí
authors.forename: Verónica
authors.initials: V
authors.lastname: Regueiro
authors.forename: Pedro
authors.initials: P
authors.lastname: Marsé
authors.forename: Joan M
authors.initials: JM
authors.lastname: Raurich
authors.forename: Jordi
authors.initials: J
authors.lastname: Ibáñez
authors.forename: Abelardo
authors.initials: A
authors.lastname: García de Lorenzo-Mateos
authors.forename: José A
authors.initials: JA
authors.lastname: Bengoechea
mesh_terms: D000328:Adult; D005260:Female; D005973:Glutamine / Q000008:administration & dosage*; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology*; D007362:Intensive Care Units; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D016037:Single-Blind Method; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis; D016896:Treatment Outcome; D014947:Wounds and Injuries / Q000188:drug therapy / Q000276:immunology*; D055815:Young Adult
chemical_list: C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D005973:Glutamine