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首页> 外文期刊>Cytokine >Interleukin-1β is internalised by viable Aggregatibacter actinomycetemcomitans biofilm and locates to the outer edges of nucleoids
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Interleukin-1β is internalised by viable Aggregatibacter actinomycetemcomitans biofilm and locates to the outer edges of nucleoids

机译：白细胞介素-1β被可行的集放线放线菌生物膜内在化并位于类核苷酸的外边缘

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摘要

The opportunistic pathogen Aggregatibacter actinomycetemcomitans causes periodontitis, which is a biofilm infection that destroys tooth-supportive tissues. Interleukin (IL)-1β, a central proinflammatory cytokine of periodontitis, is an essential first line cytokine for local inflammation that modulates the cell proliferation and anti-pathogen response of human gingival keratinocytes. Previously, we demonstrated that A. actinomycetemcomitans biofilms bind IL-1β; however, whether this binding is an active process is not known. In this study, we showed for the first time with immuno-electron microscopy that viable bacterial biofilm cells internalised IL-1β when co-cultured with an organotypic mucosa. Decreased biofilm viability hindered the ability of biofilm to sequester IL-1β and caused IL-1β leakage into the culture medium. In some A. actinomycetemcomitans cells, intracellular IL-1β localized to the outer edges of the nucleoids. We identified the DNA-binding protein HU as an IL-1β interacting protein with mass spectroscopy and showed the interaction of recombinant HU and IL-1β in vitro using enzyme-linked immunosorbent assay (ELISA). Close contact with a viable A. actinomycetemcomitans biofilm decreased the proliferation and apoptosis of human gingival keratinocytes as demonstrated using Ki-67 and the terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining, respectively. Our results suggest that viable A. actinomycetemcomitans biofilms may disturb the critical first steps of local inflammation in periodontitis by binding and internalising IL-1β. The interaction of IL-1β with conserved HU provides a potential mechanism for shaping bacterial gene expression.
机译：机会性病原体放线杆菌引起牙周炎，这是一种生物膜感染，破坏了牙齿支持组织。白细胞介素（IL）-1β是牙周炎的中枢促炎细胞因子，是调节人类牙龈角质形成细胞的细胞增殖和抗病原反应的局部炎症必不可少的一线细胞因子。以前，我们证明了放线放线杆菌的生物膜结合IL-1β。但是，此绑定是否为活动进程尚不清楚。在这项研究中，我们首次通过免疫电子显微镜观察到，当与器官型粘膜共培养时，可行的细菌生物膜细胞将IL-1β内在化。生物膜生存力的降低阻碍了生物膜螯合IL-1β的能力，并导致IL-1β泄漏到培养基中。在一些放线放线杆菌的细胞中，细胞内IL-1β定位在核苷的外边缘。我们通过质谱鉴定了DNA结合蛋白HU为IL-1β相互作用蛋白，并通过酶联免疫吸附试验（ELISA）显示了重组HU和IL-1β的相互作用。分别与Ki-67和末端脱氧核苷酸转移酶dUTP缺口末端标记法（TUNEL）染色证实，与可行的放线放线杆菌生物膜的紧密接触降低了人牙龈角质形成细胞的增殖和凋亡。我们的结果表明，可行的放线放线杆菌生物膜可能会通过结合和内化IL-1β干扰牙周炎局部炎症的关键第一步。 IL-1β与保守的HU的相互作用为塑造细菌基因表达提供了潜在的机制。

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