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体外宿主-寄生虫相互作用模型:原发性人上皮细胞的“龈下”生物膜挑战。

In vitro modeling of host-parasite interactions: the 'subgingival' biofilm challenge of primary human epithelial cells.

机构信息

Institute for Oral Biology, Section for Oral Microbiology and General Immunology, University of Zürich, Plattenstrasse 11, CH-8032 Zürich, Switzerland.

出版信息

BMC Microbiol. 2009 Dec 31;9:280. doi: 10.1186/1471-2180-9-280.

Abstract

BACKGROUND

Microbial biofilms are known to cause an increasing number of chronic inflammatory and infectious conditions. A classical example is chronic periodontal disease, a condition initiated by the subgingival dental plaque biofilm on gingival epithelial tissues. We describe here a new model that permits the examination of interactions between the bacterial biofilm and host cells in general. We use primary human gingival epithelial cells (HGEC) and an in vitro grown biofilm, comprising nine frequently studied and representative subgingival plaque bacteria.

RESULTS

We describe the growth of a mature 'subgingival' in vitro biofilm, its composition during development, its ability to adapt to aerobic conditions and how we expose in vitro a HGEC monolayer to this biofilm. Challenging the host derived HGEC with the biofilm invoked apoptosis in the epithelial cells, triggered release of pro-inflammatory cytokines and in parallel induced rapid degradation of the cytokines by biofilm-generated enzymes.

CONCLUSION

We developed an experimental in vitro model to study processes taking place in the gingival crevice during the initiation of inflammation. The new model takes into account that the microbial challenge derives from a biofilm community and not from planktonically cultured bacterial strains. It will facilitate easily the introduction of additional host cells such as neutrophils for future biofilm:host cell challenge studies. Our methodology may generate particular interest, as it should be widely applicable to other biofilm-related chronic inflammatory diseases.

摘要

背景

微生物生物膜会导致越来越多的慢性炎症和感染性疾病。一个典型的例子是慢性牙周病,这是一种由龈下牙周菌斑生物膜引起的牙龈上皮组织疾病。我们在这里描述了一种新的模型,该模型允许研究细菌生物膜与宿主细胞之间的相互作用。我们使用原代人牙龈上皮细胞(HGEC)和体外培养的生物膜,其中包含九种经常研究的代表性龈下菌斑细菌。

结果

我们描述了成熟的“龈下”体外生物膜的生长、其在发育过程中的组成、适应有氧条件的能力以及我们如何将 HGEC 单层暴露于该生物膜。用生物膜挑战宿主来源的 HGEC 会导致上皮细胞凋亡,触发促炎细胞因子的释放,并同时诱导生物膜产生的酶快速降解细胞因子。

结论

我们开发了一种体外实验模型来研究炎症起始时龈沟内发生的过程。新模型考虑到微生物的挑战来自生物膜群落,而不是浮游培养的细菌株。它将方便地引入其他宿主细胞,如中性粒细胞,用于未来的生物膜:宿主细胞挑战研究。我们的方法可能会引起特别的兴趣,因为它应该广泛适用于其他与生物膜相关的慢性炎症性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da9b/2818713/4232ec2cb910/1471-2180-9-280-1.jpg

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