TY - JOUR
T1 - Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis
AU - Hou, Yu-Chen
AU - Liu, Jun Jen
AU - Pai, Man Hui
AU - Tsou, Shung Sheng
AU - Yeh, Sung Ling
PY - 2013
Y1 - 2013
N2 - T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated cytokine expressions and inflammatory reaction in dextran sulfate sodium (DSS)-induced colitis. C57BL/6 mice received distilled water containing 3% DSS for 5 days to induce colitis, whereas the normal control (NC) group received distilled water. After induction of colitis, one of the colitis groups (DG) was intraperitoneally injected with an Ala-Gln solution (0.5 g Gln/kg/d), and the saline DSS group (DS) received an identical volume of saline. After treatment for 3 days, mice were sacrificed, and the blood and tissue samples were collected for further analysis. DSS colitis resulted in higher percentages of blood interleukin (IL)-17-secreting Th cells and greater expression of Th cell-associated cytokine messenger RNA (mRNA) in the mesenteric lymph nodes (MLN). Also, luminal immunoglobin (Ig) G, keratinocyte-derived chemokine, and macrophage chemoattractant protein-1 levels were higher in the DS group than the NC group, whereas these parameters did not differ between the DG and NC groups. The DG group had lower blood IL-17A, 17F, MLN IL-17 mRNA and macrophage percentage in the peritoneal lavage fluid than those of the DS group. These results suggest that post-treatment with Ala-Gln suppressed Th17-associated cytokine expressions, reduced macrophage infiltration into the peritoneal cavity and decreased pro-inflammatory cytokine production in the colon, thus may have attenuated inflammatory response in DSS-induced colitis.
AB - T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated cytokine expressions and inflammatory reaction in dextran sulfate sodium (DSS)-induced colitis. C57BL/6 mice received distilled water containing 3% DSS for 5 days to induce colitis, whereas the normal control (NC) group received distilled water. After induction of colitis, one of the colitis groups (DG) was intraperitoneally injected with an Ala-Gln solution (0.5 g Gln/kg/d), and the saline DSS group (DS) received an identical volume of saline. After treatment for 3 days, mice were sacrificed, and the blood and tissue samples were collected for further analysis. DSS colitis resulted in higher percentages of blood interleukin (IL)-17-secreting Th cells and greater expression of Th cell-associated cytokine messenger RNA (mRNA) in the mesenteric lymph nodes (MLN). Also, luminal immunoglobin (Ig) G, keratinocyte-derived chemokine, and macrophage chemoattractant protein-1 levels were higher in the DS group than the NC group, whereas these parameters did not differ between the DG and NC groups. The DG group had lower blood IL-17A, 17F, MLN IL-17 mRNA and macrophage percentage in the peritoneal lavage fluid than those of the DS group. These results suggest that post-treatment with Ala-Gln suppressed Th17-associated cytokine expressions, reduced macrophage infiltration into the peritoneal cavity and decreased pro-inflammatory cytokine production in the colon, thus may have attenuated inflammatory response in DSS-induced colitis.
KW - Alanyl-glutamine
KW - DSS-colitis
KW - Immunoglobin G
KW - Interleukin-17
KW - T helper cells
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UR - http://www.scopus.com/inward/citedby.url?scp=84878486032&partnerID=8YFLogxK
U2 - 10.1016/j.intimp.2013.05.004
DO - 10.1016/j.intimp.2013.05.004
M3 - Article
C2 - 23721689
AN - SCOPUS:84878486032
SN - 1567-5769
VL - 17
SP - 1
EP - 8
JO - International Immunopharmacology
JF - International Immunopharmacology
IS - 1
ER -