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

In vitro modeling of host-parasite interactions: the 'subgingival' biofilm challenge of primary human epithelial cells
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DOI:
10.1186/1471-2180-9-280
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发表时间:
2009-12-31
期刊:
影响因子:
4.2
通讯作者:
Kinane, Denis F.
Kinane, Denis F.
中科院分区:
生物学3区
文献类型:
--
作者:
Guggenheim, Bernhard;Gmuer, Rudolf;Kinane, Denis F.

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背景:已知微生物生物膜引起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,这是由牙龈上皮组织上的龈下牙菌斑生物膜引发的一种疾病。我们在这里描述了一个新的模型,允许检查细菌生物膜和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,包括九种经常被研究和代表性的牙龈下菌斑细菌。结果:我们描述了成熟的“牙龈下”体外生物膜的生长,其在发育过程中的组成,其适应有氧条件的能力,以及我们如何在体外将HGEC单层暴露于该生物膜中。用生物膜挑战宿主源性HGEC会引起上皮细胞凋亡,触发促炎细胞因子的释放,同时通过生物膜生成的酶诱导细胞因子的快速降解。结论:我们建立了一个实验性的体外模型来研究炎症开始时牙龈缝隙中发生的过程。新模型考虑到微生物挑战来自生物膜群落,而不是来自浮游培养的菌株。这将有助于引入额外的宿主细胞,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生物膜相关的慢性炎症性疾病。
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.