Neisseria meningitidis (the meningococcus) remains an important cause of human disease, including meningitis and sepsis. Adaptation to the host environment includes many interactions with specific cell surface receptors, resulting in intracellular signalling and cytoskeletal rearrangements that contribute to pathogenesis. Here, we assessed the interactions between meningococci and Fibroblast Growth Factor Receptor 1-IIIc (FGFR1-IIIc): a receptor specific to endothelial cells of the microvasculature, including that of the blood-brain barrier. We show that the meningococcus recruits FGFR1-IIIc onto the surface of human blood microvascular endothelial cells (HBMECs). Furthermore, we demonstrate that expression of FGFR1-IIIc is required for optimal invasion of HBMECs by meningococci. We show that the ability of N. meningitidis to interact with the ligand-binding domain of FGFR1-IIIc is shared with the other pathogenic Neisseria species, N. gonorrhoeae, but not with commensal bacteria including non-pathogenic Neisseria species.

脑膜炎奈瑟菌（脑膜炎球菌）仍然是人类疾病的重要原因，包括脑膜炎和败血症。对宿主环境的适应包括与特定细胞表面受体的许多相互作用，导致细胞内信号传导和细胞骨架重排，从而促进发病。在这里，我们评估了脑膜炎球菌和成纤维细胞生长因子受体 1-IIIc (FGFR1-IIIc) 之间的相互作用：一种对微血管系统内皮细胞具有特异性的受体，包括血脑屏障的内皮细胞。我们表明脑膜炎球菌将 FGFR1-IIIc 招募到人血液微血管内皮细胞 (HBMEC) 的表面。此外，我们证明 FGFR1-IIIc 的表达是脑膜炎球菌对 HBMECs 的最佳侵袭所必需的。我们证明了能力脑膜炎奈瑟氏球菌与FGFR1-IIIC的配体结合结构域与其他致病共享交互奈瑟氏球菌物种，淋病奈瑟氏球菌，但不与共生细菌包括非致病奈瑟氏球菌属物种。