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How bacterial pathogens of the gastrointestinal tract use the mucosal glyco-code to harness mucus and microbiota: New ways to study an ancient bag of tricks.
International Journal of Medical Microbiology ( IF 4.1 ) Pub Date : 2020-01-16 , DOI: 10.1016/j.ijmm.2020.151392
Christine Josenhans 1 , Johannes Müthing 2 , Lothar Elling 3 , Sina Bartfeld 4 , Herbert Schmidt 5
Affiliation  

During the last decades, the flourishing scientific field of molecular pathogenesis brought groundbreaking knowledge of the mechanisms of pathogenicity and the underlying bacterial virulence factors to cause infectious diseases. However, a major paradigm shift is currently occurring after it became increasingly evident that bacterial-host and host-host cell interactions including immune responses orchestrated by defined virulence factors are not the sole drivers of infectious disease development. Strong evidence has been collected that information and nutrient flow within complex microbial communities, as well as to and from host cells and matrices are equally important for successful infection. This particularly holds true for gastrointestinal (GI) pathogens and the GI microbiota interacting and communicating with each other as well as with the host GI mucus and mucosa. Gut-adapted pathogens appear to have developed powerful and specific strategies to interact with human GI mucus including the microbiota for nutrient acquisition, mucosal adhesion, inter-species communication and traversing the mucus barrier. This review covers the existing evidence on these topics and explores the mutual dynamics of host GI mucus, the mucosal habitat and incoming acute and chronic pathogens during GI infections. A particular focus is placed on the role of carbohydrates in diverse mucosal interaction, communication and competition processes. Novel techniques to analyze and synthesize mucus-derived carbohydrates and to generate mucus mimetics are introduced. Finally, open questions and future objectives for pathogen - host GI mucus research will be discussed.



中文翻译:

胃肠道细菌病原体如何使用粘膜糖代码来控制粘液和微生物群:研究古老方法的新方法。

在过去的几十年中,分子发病机理的蓬勃发展的科学领域带来了有关致病机理和引起传染病的潜在细菌致病因子的开创性知识。然而,在越来越明显的是细菌-宿主和宿主-细胞之间的相互作用,包括由确定的毒力因子精心策划的免疫应答,并不是引起传染病发展的唯一驱动因素之后,目前正在发生重大的范式转变。已有强有力的证据表明,复杂的微生物群落内部以及宿主细胞和基质之间的信息和营养流动对于成功感染同样重要。对于胃肠道(GI)病原体和GI微生物群以及彼此以及与宿主GI粘液和粘膜相互作用和通讯的情况尤其如此。适应肠道的病原体似乎已开发出强大且特定的策略来与人类胃肠粘液相互作用,包括用于获取营养物,粘膜黏附,种间通讯和穿越粘液屏障的微生物群。这篇综述涵盖了有关这些主题的现有证据,并探讨了胃肠道感染期间宿主胃肠道粘液,粘膜生境以及传入的急慢性病原体的相互动态。特别关注碳水化合物在各种粘膜相互作用,交流和竞争过程中的作用。介绍了分析和合成粘液来源的碳水化合物并生成粘液模拟物的新技术。最后,将讨论病原体-宿主胃肠粘液研究的悬而未决的问题和未来目标。

更新日期:2020-01-16
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