细菌脑膜炎在全球范围内依然是一个公共卫生的挑战，即便治愈也会留下严重的后遗症，像听力损伤、视觉障碍、跛足和认知缺陷等，给个人和家庭带来持久的影响。B族链球菌（GBS）是革兰阳性胞外链球菌，是引起新生儿脑膜炎的首要病原体，患儿具有高的病死率和病残率。到目前为止GBS引发脑膜炎的机制尚不清楚。我们在前期工作中发现Gb3缺失能够减少GBS感染小鼠的死亡，降低血中细菌的载荷，因此我们推测Gb3有助于GBS脑膜炎的形成。在本项目中，我们将利用小鼠模型评价Gb3在GBS致脑膜炎中的作用；利用蛋白相互作用鉴定与Gb3相互作用的细菌配体；利用CRISPR/Cas9基因编辑技术获取Gb3缺失细胞，在体外评价Gb3与GBS的相互作用。通过体内和体外探究GBS致脑膜炎的分子机制，以期为新生儿脑膜炎的预防和治疗提供新的思路。

Bacterial meningitis remains a public health challenge around the world and can also lead to serious impairments, termed “sequelae”, such as hearing loss, visual impairment, limb loss, and cognitive impairment, with lasting effects on individuals and their families. Group B streptocuccus is a Gram positive extracellular diplococcus and is the first cause of meningitis in neonates with high mortality and morbidity. Up to now, the mechanism of GBS leading to meningitis is remained unclear.In the previous work, we found that Gb3 deficiency can reduce the death of GBS-infected mice and reduce the bacterial load in blood. Therefore, we speculate that Gb3 may contribute to the development of GBS meningitis. In this project, we will use a mouse model to evaluate the role of Gb3 in GBS caused meningitis; use protein interactions to identify bacterial ligand that interact with Gb3; use CRISPR/Cas9 gene editing technology to obtain Gb3-deficient cells, and evaluate the interaction between Gb3 and GBS in vitro. Explore the molecular mechanism of GBS caused meningitis in vivo and in vitro, thus providing new insights for the prevention and treatment of meningitis in neonates through our research.