Send to

Choose Destination
Mediators Inflamm. 2014;2014:837107. doi: 10.1155/2014/837107. Epub 2014 May 7.

Glutamine supplementation attenuates expressions of adhesion molecules and chemokine receptors on T cells in a murine model of acute colitis.

Author information

Department of Surgery, National Taiwan University Hospital, Taipei 100, Taiwan.
School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan.
Department of Surgery, National Taiwan University Hospital, Taipei 100, Taiwan ; Department of Primary Care Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan.



Migration of T cells into the colon plays a major role in the pathogenesis in inflammatory bowel disease. This study investigated the effects of glutamine (Gln) supplementation on chemokine receptors and adhesion molecules expressed by T cells in mice with dextran sulfate sodium- (DSS-) induced colitis.


C57BL/6 mice were fed either a standard diet or a Gln diet replacing 25% of the total nitrogen. After being fed the diets for 5 days, half of the mice from both groups were given 1.5% DSS in drinking water to induce colitis. Mice were killed after 5 days of DSS exposure.


DSS colitis resulted in higher expression levels of P-selectin glycoprotein ligand- (PSGL-) 1, leukocyte function-associated antigen- (LFA-) 1, and C-C chemokine receptor type 9 (CCR9) by T helper (Th) and cytotoxic T (Tc) cells, and mRNA levels of endothelial adhesion molecules in colons were upregulated. Gln supplementation decreased expressions of PSGL-1, LFA-1, and CCR9 by Th cells. Colonic gene expressions of endothelial adhesion molecules were also lower in Gln-colitis mice. Histological finding showed that colon infiltrating Th cells were less in the DSS group with Gln administration.


Gln supplementation may ameliorate the inflammation of colitis possibly via suppression of T cell migration.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Hindawi Limited Icon for PubMed Central
Loading ...
Support Center