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细菌表面结构在肺炎克雷伯菌与吞噬细胞相互作用中的作用。

Role of bacterial surface structures on the interaction of Klebsiella pneumoniae with phagocytes.

机构信息

Laboratory Microbial Pathogenesis, Fundació d'Investigació Sanitària de les Illes Balears (FISIB), Bunyola, Spain.

出版信息

PLoS One. 2013;8(2):e56847. doi: 10.1371/journal.pone.0056847. Epub 2013 Feb 15.

Abstract

Phagocytosis is a key process of the immune system. The human pathogen Klebsiella pneumoniae is a well known example of a pathogen highly resistant to phagocytosis. A wealth of evidence demonstrates that the capsule polysaccharide (CPS) plays a crucial role in resistance to phagocytosis. The amoeba Dictyostelium discoideum shares with mammalian macrophages the ability to phagocytose and kill bacteria. The fact that K. pneumoniae is ubiquitous in nature and, therefore, should avoid predation by amoebae, poses the question whether K. pneumoniae employs similar means to counteract amoebae and mammalian phagocytes. Here we developed an assay to evaluate K. pneumoniae-D. discoideum interaction. The richness of the growth medium affected the threshold at which the cps mutant was permissive for Dictyostelium and only at lower nutrient concentrations the cps mutant was susceptible to predation by amoebae. Given the critical role of bacterial surface elements on host-pathogen interactions, we explored the possible contribution of the lipopolysaccharide (LPS) and outer membrane proteins (OMPs) to combat phagoyctosis by D. discoideum. We uncover that, in addition to the CPS, the LPS O-polysaccharide and the first core sugar participate in Klebsiella resistance to predation by D. discoideum. K. pneumoniae LPS lipid A decorations are also necessary to avoid predation by amoebae although PagP-dependent palmitoylation plays a more important role than the lipid A modification with aminoarabinose. Mutants lacking OMPs OmpA or OmpK36 were also permissive for D. discoideium growth. Except the LPS O-polysaccharide mutants, all mutants were more susceptible to phagocytosis by mouse alveolar macrophages. Finally, we found a correlation between virulence, using the pneumonia mouse model, and resistance to phagocytosis. Altogether, this work reveals novel K. pneumoniae determinants involved in resistance to phagocytosis and supports the notion that Dictyostelium amoebae might be useful as host model to measure K. pneumoniae virulence and not only phagocytosis.

摘要

吞噬作用是免疫系统的关键过程。人类病原体肺炎克雷伯菌是一种众所周知的对吞噬作用具有高度抗性的病原体。大量证据表明,荚膜多糖(CPS)在抵抗吞噬作用中起着至关重要的作用。变形虫盘基网柄菌与哺乳动物巨噬细胞具有吞噬和杀死细菌的能力。肺炎克雷伯菌在自然界中无处不在,因此应该避免被变形虫捕食,这就提出了一个问题,即肺炎克雷伯菌是否采用类似的手段来对抗变形虫和哺乳动物吞噬细胞。在这里,我们开发了一种评估肺炎克雷伯菌-盘基网柄菌相互作用的测定方法。生长培养基的丰富度影响了 cps 突变体对盘基网柄菌允许的阈值,只有在较低的营养浓度下,cps 突变体才容易被变形虫捕食。鉴于细菌表面元素在宿主-病原体相互作用中的关键作用,我们探索了脂多糖(LPS)和外膜蛋白(OMPs)对变形虫吞噬作用的可能贡献。我们发现,除了 CPS 外,LPS O-多糖和第一核心糖也参与了肺炎克雷伯菌抵抗变形虫捕食的作用。肺炎克雷伯菌 LPS 脂质 A 修饰对于避免变形虫捕食也是必要的,尽管 PagP 依赖性棕榈酰化比氨基阿拉伯糖修饰脂质 A 更重要。缺失 OMPs OmpA 或 OmpK36 的突变体也允许盘基网柄菌生长。除了 LPS O-多糖突变体外,所有突变体对肺泡巨噬细胞的吞噬作用都更敏感。最后,我们发现肺炎克雷伯菌的毒力与吞噬作用的抗性之间存在相关性。总的来说,这项工作揭示了肺炎克雷伯菌抵抗吞噬作用的新决定因素,并支持了变形虫可能是衡量肺炎克雷伯菌毒力而不仅仅是吞噬作用的有用宿主模型的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f7a/3574025/f97476386004/pone.0056847.g001.jpg

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