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本文引用的文献

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gp96 expression in neutrophils is critical for the onset of Escherichia coli K1 (RS218) meningitis.中性粒细胞中 gp96 的表达对于大肠杆菌 K1(RS218)脑膜炎的发作至关重要。
Nat Commun. 2011 Nov 22;2:552. doi: 10.1038/ncomms1554.
2
Bacterial Pili exploit integrin machinery to promote immune activation and efficient blood-brain barrier penetration.细菌菌毛利用整合素机制促进免疫激活和高效血脑屏障穿透。
Nat Commun. 2011 Sep 6;2:462. doi: 10.1038/ncomms1474.
3
Glycosaminoglycan binding facilitates entry of a bacterial pathogen into central nervous systems.糖胺聚糖结合有助于细菌病原体进入中枢神经系统。
PLoS Pathog. 2011 Jun;7(6):e1002082. doi: 10.1371/journal.ppat.1002082. Epub 2011 Jun 23.
4
Bacterial meningitis in the United States, 1998-2007.美国 1998-2007 年细菌性脑膜炎流行情况。
N Engl J Med. 2011 May 26;364(21):2016-25. doi: 10.1056/NEJMoa1005384.
5
Transcriptome analysis of Neisseria meningitidis in human whole blood and mutagenesis studies identify virulence factors involved in blood survival.脑膜炎奈瑟菌在人全血中的转录组分析和诱变研究鉴定了与血液存活相关的毒力因子。
PLoS Pathog. 2011 May;7(5):e1002027. doi: 10.1371/journal.ppat.1002027. Epub 2011 May 5.
6
Contribution of lethal toxin and edema toxin to the pathogenesis of anthrax meningitis.致死毒素和水肿毒素对炭疽性脑膜炎发病机制的贡献。
Infect Immun. 2011 Jul;79(7):2510-8. doi: 10.1128/IAI.00006-11. Epub 2011 Apr 25.
7
Early onset neonatal sepsis: the burden of group B Streptococcal and E. coli disease continues.早发型新生儿败血症:B 群链球菌和大肠杆菌病的负担仍在继续。
Pediatrics. 2011 May;127(5):817-26. doi: 10.1542/peds.2010-2217. Epub 2011 Apr 25.
8
Bacillus anthracis protease InhA increases blood-brain barrier permeability and contributes to cerebral hemorrhages.炭疽芽孢杆菌蛋白酶 InhA 增加血脑屏障通透性并导致脑出血。
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9
Extracellular matrix and cell signalling: the dynamic cooperation of integrin, proteoglycan and growth factor receptor.细胞外基质与细胞信号:整合素、蛋白聚糖和生长因子受体的动态协作。
J Endocrinol. 2011 May;209(2):139-51. doi: 10.1530/JOE-10-0377. Epub 2011 Feb 9.
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Molecular basis of increased serum resistance among pulmonary isolates of non-typeable Haemophilus influenzae.非典型流感嗜血杆菌肺分离株血清抗性增加的分子基础。
PLoS Pathog. 2011 Jan 6;7(1):e1001247. doi: 10.1371/journal.ppat.1001247.

边境防御:血脑屏障与细菌入侵者的较量。

Defense at the border: the blood-brain barrier versus bacterial foreigners.

机构信息

University Medical Center Utrecht, Medical Microbiology, Heidelberglaan 100, G04.614, 3584 GX Utrecht, The Netherlands.

出版信息

Future Microbiol. 2012 Mar;7(3):383-94. doi: 10.2217/fmb.12.1.

DOI:10.2217/fmb.12.1
PMID:22393891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3589978/
Abstract

Bacterial meningitis is among the top ten causes of infectious disease-related deaths worldwide, with up to half of the survivors left with permanent neurological sequelae. The blood-brain barrier (BBB), composed mainly of specialized brain microvascular endothelial cells, maintains biochemical homeostasis in the CNS by regulating the passage of nutrients, molecules and cells from the blood to the brain. Despite its highly restrictive nature, certain bacterial pathogens are able to gain entry into the CNS resulting in serious disease. In recent years, important advances have been made in understanding the molecular and cellular events that are involved in the development of bacterial meningitis. In this review, we summarize the progress made in elucidating the molecular mechanisms of bacterial BBB-crossing, highlighting common themes of host-pathogen interaction, and the potential role of the BBB in innate defense during infection.

摘要

细菌性脑膜炎是全球十大传染病相关死亡原因之一,多达一半的幸存者留有永久性神经后遗症。血脑屏障(BBB)主要由专门的脑微血管内皮细胞组成,通过调节营养物质、分子和细胞从血液进入大脑的过程,维持中枢神经系统的生化平衡。尽管 BBB 具有高度的限制性,但某些细菌病原体能够进入中枢神经系统,导致严重疾病。近年来,人们在理解参与细菌性脑膜炎发生的分子和细胞事件方面取得了重要进展。在这篇综述中,我们总结了阐明细菌穿透 BBB 的分子机制方面的进展,强调了宿主-病原体相互作用的共同主题,以及 BBB 在感染期间固有防御中的潜在作用。