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凝集素-聚糖相互作用概述:引发真菌感染和发病机制的关键事件。

An overview of lectin-glycan interactions: a key event in initiating fungal infection and pathogenesis.

作者信息

Ballal Suhas, Inamdar Shashikala R

机构信息

Department of Studies in Biochemistry, Karnatak University, Dharwad, India.

出版信息

Arch Microbiol. 2018 Apr;200(3):371-382. doi: 10.1007/s00203-018-1487-1. Epub 2018 Feb 13.

Abstract

Infections due to microfungi are of serious concern in many parts of the world. Many species of microfungi are known to cause systemic infection in human beings. Pathogenic microorganisms employ various molecular strategies for colonizing a susceptible host. Recent studies have shown the importance of lectins from microfungi that enable the pathogen to interact with the host, resulting in host immune response. These fungal lectins or adhesins show specific affinities to the glycans present on the membrane proteins or lipids. Binding of the pathogen to the receptors, probably toll-like receptors or dectins, present on the host cell surface triggers/initiates a cascade of signalling pathways, leading to the activation of transcription factors such as NF-κB resulting in the release of proinflammatory cytokines which in turn recruit cells of the immune system to the site of microbial insult to combat the pathogen or resulting in pathogenesis. In this review, we will focus on the interaction between fungal lectins and the host glycans initiating pathogenesis and how the host immune system tries to suppress the pathogenesis.

摘要

微真菌引起的感染在世界许多地区都备受关注。已知许多微真菌物种会导致人类全身感染。致病微生物采用各种分子策略来定殖易感宿主。最近的研究表明,微真菌中的凝集素很重要,它能使病原体与宿主相互作用,从而引发宿主免疫反应。这些真菌凝集素或黏附素对膜蛋白或脂质上存在的聚糖具有特异性亲和力。病原体与宿主细胞表面存在的受体(可能是Toll样受体或脱铁素)结合,会触发/启动一系列信号通路,导致转录因子如核因子κB的激活,从而释放促炎细胞因子,进而将免疫系统的细胞募集到微生物侵害部位以对抗病原体,或导致发病机制。在这篇综述中,我们将重点关注引发发病机制的真菌凝集素与宿主聚糖之间的相互作用,以及宿主免疫系统如何试图抑制发病机制。

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