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非ulosonic酸有助于口腔细菌的致病性。

Nonulosonic acids contribute to the pathogenicity of the oral bacterium .

作者信息

Bloch Susanne, Tomek Markus B, Friedrich Valentin, Messner Paul, Schäffer Christina

机构信息

Department of NanoBiotechnology, NanoGlycobiology unit, Universität für Bodenkultur Wien, Muthgasse 11, 1190 Vienna, Austria.

出版信息

Interface Focus. 2019 Apr 6;9(2):20180064. doi: 10.1098/rsfs.2018.0064. Epub 2019 Feb 15.

DOI:10.1098/rsfs.2018.0064
PMID:30842870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6388019/
Abstract

Periodontitis is a polymicrobial, biofilm-caused, inflammatory disease affecting the tooth-supporting tissues. It is not only the leading cause of tooth loss worldwide, but can also impact systemic health. The development of effective treatment strategies is hampered by the complicated disease pathogenesis which is best described by a polymicrobial synergy and dysbiosis model. This model classifies the Gram-negative anaerobe as a periodontal pathogen, making it a prime candidate for interference with the disease. employs a protein -glycosylation system that enables high-density display of nonulosonic acids via the bacterium's two-dimensional crystalline cell surface layer. Nonulosonic acids are sialic acid-like sugars which are well known for their pivotal biological roles. This review summarizes the current knowledge of s unique cell envelope with a focus on composition, biosynthesis and functional implications of the cell surface -glycan. We have obtained evidence that glycobiology affects the bacterium's immunogenicity and capability to establish itself in the polymicrobial oral biofilm. Analysis of the genomes of different isolates revealed that complex protein -glycosylation involving nonulosonic acids is a hallmark of pathogenic strains and, thus, constitutes a valuable target for the design of novel anti-infective strategies to combat periodontitis.

摘要

牙周炎是一种由多种微生物引起的生物膜性炎症疾病,会影响牙齿支持组织。它不仅是全球牙齿缺失的主要原因,还会影响全身健康。复杂的疾病发病机制阻碍了有效治疗策略的发展,这种发病机制最好用多微生物协同和生态失调模型来描述。该模型将革兰氏阴性厌氧菌归类为牙周病原体,使其成为干预该疾病的主要候选对象。[该细菌]采用一种蛋白质糖基化系统,能够通过细菌的二维晶体细胞表面层高密度展示非ulosonic酸。非ulosonic酸是类似唾液酸的糖类,因其关键的生物学作用而闻名。本综述总结了关于[该细菌]独特细胞包膜的当前知识,重点关注细胞表面聚糖的组成、生物合成和功能意义。我们已经获得证据表明,糖生物学会影响该细菌的免疫原性及其在多微生物口腔生物膜中定植的能力。对不同[细菌]分离株基因组的分析表明,涉及非ulosonic酸的复杂蛋白质糖基化是致病菌株的一个标志,因此,构成了设计新型抗感染策略以对抗牙周炎的一个有价值的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/6f86a09176b5/rsfs20180064-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/201a1d727fcc/rsfs20180064-g1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/6f86a09176b5/rsfs20180064-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/201a1d727fcc/rsfs20180064-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/8142a2b97af0/rsfs20180064-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/07e53f4c8986/rsfs20180064-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a2/6388019/d5be968fdd5a/rsfs20180064-g4.jpg
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2
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