| 摘要: | 小腸上皮淋巴細胞(intraepithelial lymphocytes, IEL) 大多為γδ T細胞，在小腸是重要的免疫細胞。本研究探討麩醯胺(glutamine, GLN) 對敗血症小鼠其細胞激素和免疫調節因子基因表現的影響。小鼠隨機分組為控制組(normal control, NC)、敗血症給予生理食鹽水(sepsis with saline, SS)，以及敗血症給予每公斤體重0.75公克GLN (sepsis with 0.75 g/ kg GLN, SG)的組別。實驗以盲腸結紮穿刺手術引發敗血症，手術後一小時尾靜脈注射單一劑量生理食鹽水或GLN，在引發敗血症後12小時犧牲小鼠。結果顯示敗血症小鼠小腸IEL γδ T細胞數量減少，其interferon-γ、tumor necrosis factor-α、interleukin (IL)-4、IL-13、IL-17、retinoid-acid receptor-related orphan receptor gamma t (RORγt) 和complement 5a receptor (C5aR) messenger (m)RNA表現量增加。然而，給予GLN之敗血症小鼠小腸IEL γδ T細胞促發炎細胞激素和抗發炎細胞激素基因mRNA和細胞凋亡之表現量減少，並且增加IL-7 receptor表現量。切片結果小腸上皮細胞的損傷在SG組比SS組輕微。本研究表示在敗血症初期注射單一劑量GLN可以促進小腸IEL γδ T細胞生長、降低細胞凋亡，並降低發炎介質表現，進而改善敗血症對小腸上皮組織造成的傷害。
Intestinal intraepithelial lymphocytes (IEL) are rich in γδ T-cells, and γδT-cells play an important role in immune surveillance of the intestines. This study investigated the effect of glutamine (GLN) on cytokines and immune regulatory factor gene expressions in septic mice. Mice were randomly assigned to a normal (NC) group, a sepsis with saline (SS) group, or a sepsis with 0.75 g GLN/kg body weight (SG) group. Sepsis was induced by cecal ligation and puncture (CLP). Saline or GLN was given once via a tail vein 1 h after CLP. Mice were sacrificed 12 h after CLP. The results showed that sepsis resulted in lower intestinal IEL γδT-cells, higher messenger (m)RNA expressions of interferon-γ, tumor necrosis factor-α, interleukin (IL)-4, IL-13, IL-17, retinoid-acid receptor-related orphan receptor gamma t (RORγt), and complement 5a receptor (C5aR) by intestinal IEL γδT-cells. These immunomodulatory mediator genes and intestinal IEL γδT-cells apoptosis exhibited decreases, while IL-7 receptor expression increased in septic group with GLN administration. The histological findings also showed that damage to intestinal epithelial cells was less severe than that of the SG group. These results suggest that GLN administered after the early stage of sepsis prevented apoptosis of intestinal IEL γδT-cells, and downregulated γδT-cell-expressed inflammatory mediators, that may consequently ameliorate the severity of sepsis-induced intestinal epithelial injury. |
