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幽门螺杆菌中的脂多糖结构与生物合成

Lipopolysaccharide Structure and Biosynthesis in Helicobacter pylori.

作者信息

Li Hong, Liao Tingting, Debowski Aleksandra W, Tang Hong, Nilsson Hans-Olof, Stubbs Keith A, Marshall Barry J, Benghezal Mohammed

机构信息

West China Marshall Research Centre for Infectious Diseases, Centre of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, 610041, China.

Helicobacter pylori Research Laboratory, School of Pathology & Laboratory Medicine, Marshall Centre for Infectious Disease Research and Training, The University of Western Australia, M504, L Block, QEII Medical Centre, Nedlands, WA 6009, Australia.

出版信息

Helicobacter. 2016 Dec;21(6):445-461. doi: 10.1111/hel.12301. Epub 2016 Mar 2.

DOI:10.1111/hel.12301
PMID:26934862
Abstract

This review covers the current knowledge and gaps in Helicobacter pylori lipopolysaccharide (LPS) structure and biosynthesis. H. pylori is a Gram-negative bacterium which colonizes the luminal surface of the human gastric epithelium. Both a constitutive alteration of the lipid A preventing TLR4 elicitation and host mimicry of the Lewis antigen decorated O-antigen of H. pylori LPS promote immune escape and chronic infection. To date, the complete structure of H. pylori LPS is not available, and the proposed model is a linear arrangement composed of the inner core defined as the hexa-saccharide (Kdo-LD-Hep-LD-Hep-DD-Hep-Gal-Glc), the outer core composed of a conserved trisaccharide (-GlcNAc-Fuc-DD-Hep-) linked to the third heptose of the inner core, the glucan, the heptan and a variable O-antigen, generally consisting of a poly-LacNAc decorated with Lewis antigens. Although the glycosyltransferases (GTs) responsible for the biosynthesis of the H. pylori O-antigen chains have been identified and characterized, there are many gaps in regard to the biosynthesis of the core LPS. These limitations warrant additional mutagenesis and structural studies to obtain the complete LPS structure and corresponding biosynthetic pathway of this important gastric bacterium.

摘要

本综述涵盖了幽门螺杆菌脂多糖(LPS)结构与生物合成方面的现有知识及空白。幽门螺杆菌是一种革兰氏阴性菌,定殖于人类胃上皮的管腔表面。脂多糖A的组成性改变可阻止Toll样受体4(TLR4)的激活,而幽门螺杆菌脂多糖上装饰有Lewis抗原的O抗原的宿主模拟物则促进免疫逃逸和慢性感染。迄今为止,幽门螺杆菌脂多糖的完整结构尚未明确,目前提出的模型是一种线性排列,由定义为六糖(Kdo-LD-Hep-LD-Hep-DD-Hep-Gal-Glc)的内核、与内核第三个庚糖相连的由保守三糖(-GlcNAc-Fuc-DD-Hep-)组成的外核、葡聚糖、庚聚糖和可变O抗原组成,该可变O抗原通常由装饰有Lewis抗原的多聚乳糖胺组成。尽管已鉴定并表征了负责幽门螺杆菌O抗原链生物合成的糖基转移酶(GTs),但在核心脂多糖的生物合成方面仍存在许多空白。这些局限性需要进一步开展诱变和结构研究,以获得这种重要胃部细菌的完整脂多糖结构及相应的生物合成途径。

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