Pretreatment with alanyl-glutamine suppresses T-helper-cell-associated cytokine expression and reduces inflammatory responses in mice with acute DSS-induced colitis

J Nutr Biochem. 2012 Sep;23(9):1092-9. doi: 10.1016/j.jnutbio.2011.06.002. Epub 2011 Dec 1.

Abstract

T-helper (Th) cells play a major role in initiating and shaping the pathologic response in inflammatory bowel disease (IBD). Glutamine (GLN) is a nutrient with immune-modulating effects. This study investigated the effect of GLN on cytokine expressions and inflammatory responses of three subsets of Th cells in dextran sulfate sodium (DSS)-induced IBD. There were one normal control (NC) and two DSS groups. Mice in the DSS groups drank distilled water containing 3% DSS for 5 days, whereas the NC group received distilled water. Mice in the G-DSS group were given intraperitoneal injection of 0.5 g GLN/kg/d for 3 days before receiving DSS water. The other DSS group (C-DSS) received an identical amount of amino acid solution without GLN. After induction of IBD, the mice were allowed to recover for 3 days and then were sacrificed. Blood and colon samples were collected for further analysis. The C-DSS group had higher percentages of blood interleukin (IL)-17A, IL-17F, IL-22, IL-4 and interferon-γ than the NC group. The G-DSS group had lower Th1/Th17/Th2 cytokine expressions, which showed no differences from the NC group. Plasma haptoglobin, colon immunoglobin G and chemokine levels and myeloperoxidase activities were higher in the DSS groups than the NC group. These parameters were significantly lower in the G-DSS than the C-DSS group. These results suggest that pretreatment with GLN suppressed Th-associated cytokine expressions and may consequently reduce inflammatory mediator production and leukocyte infiltration into tissues, thus ameliorating the severity of acute DSS-induced colitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
  • Colitis / blood
  • Colitis / drug therapy
  • Colitis / immunology
  • Colitis / physiopathology
  • Colitis, Ulcerative / etiology
  • Colitis, Ulcerative / prevention & control
  • Colon / drug effects*
  • Colon / immunology
  • Colon / metabolism
  • Colon / pathology
  • Cytokines / blood*
  • Cytokines / metabolism
  • Dextran Sulfate
  • Dipeptides / administration & dosage
  • Dipeptides / therapeutic use*
  • Disease Models, Animal
  • Down-Regulation / drug effects*
  • Haptoglobins / analysis
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / pathology
  • Inflammatory Bowel Diseases / physiopathology
  • Inflammatory Bowel Diseases / prevention & control*
  • Injections, Intraperitoneal
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Peroxidase / metabolism
  • Severity of Illness Index
  • T-Lymphocytes, Helper-Inducer / drug effects*
  • T-Lymphocytes, Helper-Inducer / immunology
  • T-Lymphocytes, Helper-Inducer / metabolism
  • T-Lymphocytes, Helper-Inducer / pathology

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Cytokines
  • Dipeptides
  • Haptoglobins
  • Dextran Sulfate
  • Peroxidase
  • alanylglutamine