Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, 1-1 Idaigaoka-Hasamamachi, Yufu, Oita, Japan.
Surg Today. 2010;40(2):137-45. doi: 10.1007/s00595-009-4033-6. Epub 2010 Jan 28.
Recent studies have increased our understanding of the important role that the immune system plays in ischemia-reperfusion (I/R) injury. Although dendritic cells (DCs) are important regulators of intestinal immunity, their role in the response to intestinal I/R injury is not well understood. The aim of this study was to determine whether I/R injury affects DC infiltration into the intestinal barrier.
Wistar rats were subjected to I/R injury or a sham operation. Dendritic cells were visualized by immunohistochemistry, and after 12 h of reperfusion protein levels for nucleotide-binding oligomerization domain protein 2 (NOD2), high-mobility group box 1 (HMGB1), and Toll-like receptor 4 (TLR4) were assayed by Western blotting.
The number of DCs increased at the small intestine barrier in response to intestinal I/R. A Western blot analysis of small intestinal tissue revealed that levels of NOD2, HMGB1, and TLR4 protein increased in rats subjected to I/R injury in comparison to control rats.
These results suggest that intestinal I/R increases the infiltration of DCs into the small intestine, thus potentially involving the upregulation of NOD2, HMGB1, and TLR4. Therefore, intestinal I/R might activate DCs through NOD2 and HMGB1.
最近的研究增加了我们对免疫系统在缺血再灌注（I/R）损伤中所起的重要作用的理解。尽管树突状细胞（DCs）是肠道免疫的重要调节剂，但它们在肠道 I/R 损伤反应中的作用尚不清楚。本研究旨在确定 I/R 损伤是否会影响 DC 浸润肠道屏障。
Wistar 大鼠接受 I/R 损伤或假手术。通过免疫组织化学观察树突状细胞，并在再灌注 12 小时后通过 Western blot 测定核苷酸结合寡聚化结构域蛋白 2（NOD2）、高迁移率族蛋白 B1（HMGB1）和 Toll 样受体 4（TLR4）的蛋白水平。
肠道 I/R 导致小肠屏障处的 DC 数量增加。对小肠组织的 Western blot 分析表明，与对照组大鼠相比，I/R 损伤大鼠的 NOD2、HMGB1 和 TLR4 蛋白水平增加。
这些结果表明，肠道 I/R 增加了 DC 向小肠的浸润，从而可能涉及 NOD2、HMGB1 和 TLR4 的上调。因此，肠道 I/R 可能通过 NOD2 和 HMGB1 激活 DC。
