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糖胺聚糖结合有助于细菌病原体进入中枢神经系统。

Glycosaminoglycan binding facilitates entry of a bacterial pathogen into central nervous systems.

机构信息

Glycobiology Research and Training Center, University of California, San Diego, La Jolla, California, United States of America.

出版信息

PLoS Pathog. 2011 Jun;7(6):e1002082. doi: 10.1371/journal.ppat.1002082. Epub 2011 Jun 23.

DOI:10.1371/journal.ppat.1002082
PMID:21731486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3121876/
Abstract

Certain microbes invade brain microvascular endothelial cells (BMECs) to breach the blood-brain barrier (BBB) and establish central nervous system (CNS) infection. Here we use the leading meningitis pathogen group B Streptococcus (GBS) together with insect and mammalian infection models to probe a potential role of glycosaminoglycan (GAG) interactions in the pathogenesis of CNS entry. Site-directed mutagenesis of a GAG-binding domain of the surface GBS alpha C protein impeded GBS penetration of the Drosophila BBB in vivo and diminished GBS adherence to and invasion of human BMECs in vitro. Conversely, genetic impairment of GAG expression in flies or mice reduced GBS dissemination into the brain. These complementary approaches identify a role for bacterial-GAG interactions in the pathogenesis of CNS infection. Our results also highlight how the simpler yet genetically conserved Drosophila GAG pathways can provide a model organism to screen candidate molecules that can interrupt pathogen-GAG interactions for future therapeutic applications.

摘要

某些微生物侵入脑微血管内皮细胞 (BMEC)，破坏血脑屏障 (BBB)，从而引发中枢神经系统 (CNS) 感染。在这里，我们使用主要的脑膜炎病原体 B 型链球菌 (GBS) 以及昆虫和哺乳动物感染模型，探究糖胺聚糖 (GAG) 相互作用在 CNS 进入发病机制中的潜在作用。通过对表面 GBS α C 蛋白上 GAG 结合域的定点突变，阻碍了 GBS 在体内穿透果蝇 BBB，并减少了 GBS 在体外对人 BMEC 的黏附和侵袭。相反，在果蝇或小鼠中遗传削弱 GAG 的表达，减少了 GBS 向大脑的扩散。这些互补方法确定了细菌-GAG 相互作用在 CNS 感染发病机制中的作用。我们的研究结果还强调了简单但遗传上保守的果蝇 GAG 途径如何为筛选候选分子提供模型生物，这些候选分子可以干扰病原体-GAG 相互作用，为未来的治疗应用提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/88da35a4399b/ppat.1002082.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/d16f21f0d0f1/ppat.1002082.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/603390b8b091/ppat.1002082.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/88da35a4399b/ppat.1002082.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/d16f21f0d0f1/ppat.1002082.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/603390b8b091/ppat.1002082.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2cb/3121876/88da35a4399b/ppat.1002082.g003.jpg

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