Meningitis outcome is associated with the severity of inflammation in the subarachnoid space and that the outcome can be improved through anti-inflammation. However, a comprehensive understanding of the molecular basis underlying inflammatory responses in meningitis remains enigmatic. In the current study, we sought to determine the molecular mechanism of TLR7/NF-κB on the development of meningitis in children. Cerebrospinal fluid of patients with meningitis and children with simple febrile convulsions was collected, and meningitis mouse model was induced. TLR7 expression was determined in the serum of meningitis model mice and the cerebrospinal fluid of patients using RT-qPCR and Western blot. Afterwards, loss- and gain- function assays were conducted to determine the functional role of TLR7 in meningitis mouse model. The level of procalcitonin (PCT) and the number of bacterial colonies in the serum were analyzed. ELISA was used to detect the expression of inflammatory factors. Upregulated level of TLR7 was observed in patients and mice with meningitis. Inhibiting the expression of TLR7 inhibited the development of meningitis. Overexpressing TLR7 can activate the NF-κB signaling pathway and promote mouse meningitis. NF-κB signaling pathway inhibitor reversed promotion of meningitis caused by TLR7 activation. Our study provides evidence that TLR7 elevation can activate the NF-κB signaling pathway and promote meningitis in mice.

脑膜炎的结果与蛛网膜下腔炎症的严重程度有关，并且可以通过抗炎来改善结果。然而，对脑膜炎炎症反应的分子基础的全面了解仍然是个谜。在目前的研究中，我们试图确定 TLR7/NF-κB 对儿童脑膜炎发展的分子机制。收集脑膜炎患者和单纯性高热惊厥患儿的脑脊液，建立脑膜炎小鼠模型。使用RT-qPCR和Western印迹测定脑膜炎模型小鼠血清和患者脑脊液中TLR7的表达。之后，进行损失和获得功能测定以确定 TLR7 在脑膜炎小鼠模型中的功能作用。分析血清中降钙素原（PCT）水平和细菌菌落数。采用ELISA检测炎症因子的表达。在脑膜炎患者和小鼠中观察到 TLR7 水平上调。抑制TLR7的表达抑制了脑膜炎的发展。过表达 TLR7 可以激活 NF-κB 信号通路并促进小鼠脑膜炎。NF-κB 信号通路抑制剂逆转了 TLR7 激活引起的脑膜炎的促进作用。我们的研究提供了证据表明 TLR7 升高可以激活 NF-κB 信号通路并促进小鼠脑膜炎。抑制TLR7的表达抑制了脑膜炎的发展。过表达 TLR7 可以激活 NF-κB 信号通路并促进小鼠脑膜炎。NF-κB 信号通路抑制剂逆转了 TLR7 激活引起的脑膜炎的促进作用。我们的研究提供了证据表明 TLR7 升高可以激活 NF-κB 信号通路并促进小鼠脑膜炎。抑制TLR7的表达抑制了脑膜炎的发展。过表达 TLR7 可以激活 NF-κB 信号通路并促进小鼠脑膜炎。NF-κB 信号通路抑制剂逆转了 TLR7 激活引起的脑膜炎的促进作用。我们的研究提供了证据表明 TLR7 升高可以激活 NF-κB 信号通路并促进小鼠脑膜炎。