空肠弯曲杆菌和感染后自身免疫性疾病：糖生物学概念证明,ACS Infectious Diseases

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空肠弯曲杆菌和感染后自身免疫性疾病：糖生物学概念证明
ACS Infectious Diseases ( IF 4.0 ) Pub Date : 2022-09-22 , DOI: 10.1021/acsinfecdis.2c00397
Richard A Stein ₁

Affiliation

聚糖是最多样化的大分子群之一，是所有细胞中普遍存在的成分，具有许多关键功能，包括微生物与其宿主之间的相互作用。作为研究宿主-病原体相互作用的最佳模型生物之一，胃肠道病原体空肠弯曲杆菌将大量资源用于糖基化，并展示出多种多样的表面糖衣展示。第一个描述 N 连接糖基化的细菌， C . jejuni可以通过O额外修饰蛋白质-连接的糖基化，具有对毒力很重要的细胞外荚膜多糖，代表 Penner 血清分型方案的主要决定因素，并具有参与定植、存活、炎症和免疫逃避等过程的外膜脂寡糖。除了引起胃肠道疾病和肠外感染外，空肠弯曲杆菌还与感染后自身免疫性神经病有关，其中吉兰-巴利综合征 (GBS) 和米勒费雪综合征 (MFS) 是特征最为广泛的疾病。当特定的细菌表面脂寡糖模仿宿主神经系统中的神经节苷脂时，就会发生这些感染后自身免疫性神经病。空肠弯曲杆菌为分子模拟参与自身免疫性疾病的发病机制以及细菌多态性塑造感染后自身免疫性神经病的临床表现的能力提供了第一个概念证明。以阐明空肠弯曲杆菌-GBS 联系的机制细节而告终的科学之旅是微生物学、结构生物学、糖生物学、遗传学和免疫学等多个领域的贡献的结果，并为审问其他实例提供了一个鼓舞人心的重要例子分子模拟及其在自身免疫性疾病中的作用。

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Campylobacter jejuni and Postinfectious Autoimmune Diseases: A Proof of Concept in Glycobiology

Glycans, one of the most diverse groups of macromolecules, are ubiquitous constituents of all cells and have many critical functions, including the interaction between microbes and their hosts. One of the best model organisms to study the host–pathogen interaction, the gastrointestinal pathogen Campylobacter jejuni dedicates extensive resources to glycosylation and exhibits a diverse array of surface sugar-coated displays. The first bacterium where N-linked glycosylation was described, C. jejuni can additionally modify proteins by O-linked glycosylation, has extracellular capsular polysaccharides that are important for virulence and represent the major determinant of the Penner serotyping scheme, and has outer membrane lipooligosaccharides that participate in processes such as colonization, survival, inflammation, and immune evasion. In addition to causing gastrointestinal disease and extraintestinal infections, C. jejuni was also linked to postinfectious autoimmune neuropathies, of which Guillain–Barré syndrome (GBS) and Miller Fisher syndrome (MFS) are the most extensively characterized ones. These postinfectious autoimmune neuropathies occur when specific bacterial surface lipooligosaccharides mimic gangliosides in the host nervous system. C. jejuni provided the first proof of concept for the involvement of molecular mimicry in the pathogenesis of an autoimmune disease and, also, for the ability of a bacterial polymorphism to shape the clinical presentation of the postinfectious autoimmune neuropathy. The scientific journey that culminated with elucidating the mechanistic details of the C. jejuni–GBS link was the result of contributions from several fields, including microbiology, structural biology, glycobiology, genetics, and immunology and provides an inspiring and important example to interrogate other instances of molecular mimicry and their involvement in autoimmune disease.

更新日期：2022-09-22

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