Institute for Glycomics, Griffith University, Gold Coast QLD, Australia.
Front Cell Infect Microbiol. 2012 Feb 14;2:9. doi: 10.3389/fcimb.2012.00009. eCollection 2012.
Glycan based interactions between host and pathogen are critical in many bacterial and viral diseases. Glycan interactions range from initial receptor based adherence to protecting the infective agent from the host's immune response through molecular mimicry. Campylobacter jejuni is an ideal model for studying the role of glycans in host-pathogen interactions, as well as the role of bacterial surface glycoconjugates in infection. Using glycan array analysis, C. jejuni has been shown to interact with a wide range of host glycoconjugates. Mannose and sialic acid residues appear to play a role in initial interactions between host and pathogen following environmental exposure, whereas fucose and galactose based interactions are likely to be required for prolonged colonization. Other studies have highlighted potential decoy receptor type interactions between host's intestinal mucins and C. jejuni, demonstrating the importance of host glycoproteins as defense against C. jejuni infection as well as the role for glycoconjugates found in human breast milk in protection of breast feeding infants from infection with C. jejuni. C. jejuni can produce N- and O-linked glycoproteins, capsular polysaccharide (CPS) and/or lipooligosaccharide (LOS) which results in C. jejuni presenting its own diverse sugar coated displays on the cell surface. Bacterial glycans play an important and versatile role in infection and disease. Of these, the best understood is the molecular mimicry of human gangliosides presented by C. jejuni's LOS and its link to the onset of autoimmune neuropathies such as the Guillain Barrè syndrome (GBS). However, the role of glycoconjugates presented by C. jejuni extends beyond expression of sialylated ganglioside structures involved in initiation of GBS. Expression of surface glycans by C. jejuni may also relate to the ability of this organism to interact with the glycoproteins for initial host-pathogen interactions and continued infectivity.
宿主与病原体之间的糖基相互作用在许多细菌和病毒疾病中至关重要。糖基相互作用范围从最初基于受体的粘附到通过分子模拟来保护感染剂免受宿主免疫反应的影响。空肠弯曲菌是研究糖基在宿主-病原体相互作用中的作用以及细菌表面糖缀合物在感染中的作用的理想模型。通过糖基阵列分析,已经表明空肠弯曲菌与广泛的宿主糖缀合物相互作用。甘露糖和唾液酸残基似乎在环境暴露后宿主与病原体之间的初始相互作用中起作用,而岩藻糖和半乳糖基相互作用可能是长时间定植所必需的。其他研究强调了宿主肠道粘蛋白和空肠弯曲菌之间潜在的诱饵受体类型相互作用,证明了宿主糖蛋白作为防御空肠弯曲菌感染的重要性,以及人乳中发现的糖缀合物在保护母乳喂养婴儿免受空肠弯曲菌感染中的作用。空肠弯曲菌可以产生 N-和 O-连接的糖蛋白、荚膜多糖 (CPS) 和/或脂寡糖 (LOS),这导致空肠弯曲菌在细胞表面呈现出自身多样化的糖包被展示。细菌糖在感染和疾病中起着重要而多样的作用。其中,最被理解的是空肠弯曲菌 LOS 呈现的人类神经节苷脂的分子模拟及其与自身免疫性神经病(如格林-巴利综合征 (GBS))发病的联系。然而,空肠弯曲菌呈现的糖缀合物的作用不仅限于参与 GBS 发病的唾液酸化神经节苷脂结构的表达。空肠弯曲菌表面糖的表达也可能与该生物体与糖蛋白相互作用以进行初始宿主-病原体相互作用和持续感染性有关。