Institute of Neuropathology, University of Göttingen, Robert Koch Str. 40, D-37075 Göttingen, Germany.
Neurosci Lett. 2010 Sep 20;482(1):17-20. doi: 10.1016/j.neulet.2010.06.078. Epub 2010 Jul 3.
Stimulation of murine primary microglia with Toll-like receptor (TLR) agonists enhances their ability to phagocytose and kill bacteria. Here we show that the viral TLR3 agonist poly(I:C) stimulates the release of cyto-/chemokines and nitric oxide by microglia. Poly(I:C) increases microglial phagocytosis and intracellular killing of Escherichia coli K1, a pathogenic encapsulated bacterial strain, after 30 and 90 min of co-incubation. Stimulation with a viral epitope may strengthen the resistance of the brain to bacterial infections in vivo. Our data encourage animal experiments with poly(I:C) derivatives to assess whether this approach can increase the resistance of the CNS against bacterial infections.
用 Toll 样受体 (TLR) 激动剂刺激小鼠原代小胶质细胞可增强其吞噬和杀死细菌的能力。在这里，我们发现病毒 TLR3 激动剂聚肌苷酸（poly(I:C)）可刺激小胶质细胞释放细胞因子/趋化因子和一氧化氮。在共孵育 30 和 90 分钟后，poly(I:C)增加了小胶质细胞对致病性荚膜细菌大肠杆菌 K1 的吞噬作用和细胞内杀伤作用。病毒表位的刺激可能会增强大脑对体内细菌感染的抵抗力。我们的数据鼓励使用 poly(I:C)衍生物进行动物实验，以评估这种方法是否可以提高中枢神经系统对细菌感染的抵抗力。
