Wang Jianjun, Deng Zhiyong, Wang Zeyou, Wu Jianhong, Gu Tao, Jiang Yibiao, Li Guangxin
Department of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University Kunshan 215300, People's Republic of China.
Department of Clinical Laboratory, The Second Xiangya Hospital of Central South University Changsha 410000, People's Republic of China.
Am J Transl Res. 2016 Sep 15;8(9):3700-3709. eCollection 2016.
Exosomes containing microRNA-155 act as molecule carriers during immune cell-cell communication and play an important role in the inflammatory response of infection macrophages. Previous reports have found that miR-155 was over-expressed in infection macrophages, but the significance of which is still unknown. In this study, we analyzed the impact of miR-155 loaded in exosomes derived from macrophages to the inflammatory response of infection macrophages and possible mechanisms. We found that miR-155 promoted the expression of inflammatory cytokines including TNF-a, IL-6, IL-23, but also increased the expression of CD40, CD63, CD81, and MCH-I. Meanwhile, inflammatory signal pathways proteins, such as MyD88, NF-κB in infection macrophages were down-regulated due to the over-expression of miR-155. Experiments or revealed that miR-155 promoted macrophages to inhibit or kill by regulating the inflammatory response of cells to prevent the gastritis caused by infection. These findings contribute to the understanding of miR-155 contained in exosomes in inflammatory responses of infection macrophages.
含有微小RNA - 155的外泌体在免疫细胞间通讯过程中充当分子载体，并在感染巨噬细胞的炎症反应中发挥重要作用。先前的报道发现，miR - 155在感染巨噬细胞中过度表达，但其意义仍不清楚。在本研究中，我们分析了巨噬细胞来源的外泌体中装载的miR - 155对感染巨噬细胞炎症反应的影响及其可能机制。我们发现，miR - 155不仅促进了包括TNF - a、IL - 6、IL - 23在内的炎性细胞因子的表达，还增加了CD40、CD63、CD81和MCH - I的表达。同时，由于miR - 155的过度表达，感染巨噬细胞中的炎性信号通路蛋白，如MyD88、NF - κB被下调。实验或显示，miR - 155通过调节细胞的炎症反应促进巨噬细胞抑制或杀死，以预防感染引起的胃炎。这些发现有助于理解外泌体中包含的miR - 155在感染巨噬细胞炎症反应中的作用。
