Kim Kwang Sik
Division of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Park 256, Baltimore, MD 21287-7609, USA.
J Infect Dis. 2002 Dec 1;186 Suppl 2:S220-4. doi: 10.1086/344284.
A major contributing factor to high mortality and morbidity associated with bacterial meningitis is the incomplete understanding of the pathogenesis of this disease: It is unclear how circulating bacteria cross the blood-brain barrier (BBB). Recent studies with Escherichia coli K1 show that successful traversal of the BBB requires a high degree of bacteremia, invasion of brain microvascular endothelial cells (BMEC), host cell actin cytoskeleton rearrangements and related signaling pathways, and traversal of the BBB as live bacteria. Several microbial determinants such as the K1 capsule, OmpA, Ibe proteins, AslA, TraJ, and CNF1 contribute to BMEC invasion. Of interest, E. coli K1 trafficking mechanisms differ from those of other meningitis-causing bacteria such as Listeria monocytogenes and group B streptococcus. Complete understanding of bacteria-BMEC interactions contributing to translocation of the BBB should assist in developing novel strategies to prevent bacterial meningitis.
目前尚不清楚循环细菌如何穿过血脑屏障(BBB)。最近对大肠杆菌K1的研究表明,成功穿越血脑屏障需要高度菌血症、侵袭脑微血管内皮细胞(BMEC)、宿主细胞肌动蛋白细胞骨架重排及相关信号通路,以及作为活细菌穿越血脑屏障。几种微生物决定因素,如K1荚膜、OmpA、Ibe蛋白、AslA、TraJ和CNF1,有助于BMEC侵袭。有趣的是,大肠杆菌K1的转运机制不同于其他引起脑膜炎的细菌,如单核细胞增生李斯特菌和B族链球菌。全面了解导致血脑屏障易位的细菌与BMEC的相互作用,应有助于制定预防细菌性脑膜炎的新策略。