Department of Surgery, National Taiwan University Hospital, Taipei 100, Taiwan.
School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan.
Mediators Inflamm. 2014;2014:837107. doi: 10.1155/2014/837107. Epub 2014 May 7.
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.
T 细胞向结肠迁移在炎症性肠病的发病机制中起着重要作用。本研究探讨了谷氨酰胺(Gln)补充对葡聚糖硫酸钠(DSS)诱导结肠炎小鼠 T 细胞表达趋化因子受体和黏附分子的影响。
C57BL/6 小鼠分别喂食标准饮食或 Gln 饮食,用 Gln 饮食替代总氮的 25%。喂食饮食 5 天后,两组各有一半的小鼠给予饮用水中的 1.5% DSS 诱导结肠炎。DSS 暴露 5 天后处死小鼠。
DSS 结肠炎导致 Th 和细胞毒性 T(Tc)细胞上 P 选择素糖蛋白配体-1(PSGL-1)、白细胞功能相关抗原-1(LFA-1)和 C-C 趋化因子受体 9(CCR9)的表达水平升高,结肠内皮黏附分子的 mRNA 水平上调。Gln 补充可降低 Th 细胞上的 PSGL-1、LFA-1 和 CCR9 的表达。结肠炎小鼠结肠内皮黏附分子的基因表达也较低。组织学发现,给予 Gln 后 DSS 组结肠浸润的 Th 细胞减少。
Gln 补充可能通过抑制 T 细胞迁移来改善结肠炎的炎症。