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首页> 外文期刊>Infection and immunity >Gingival Epithelial Cell Transcriptional Responses to Commensal and Opportunistic Oral Microbial Species
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Gingival Epithelial Cell Transcriptional Responses to Commensal and Opportunistic Oral Microbial Species

机译：牙龈上皮细胞转录应答的共生和机会口腔微生物物种。

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Transcriptional profiling and ontology tools were utilized to define the biological pathways of gingival epithelial cells modulated by coculture with the oral commensal Streptococcus gordonii and the opportunistic commensal Fusobacterium nucleatum. Overall, F. nucleatum and S. gordonii perturbed the gingival epithelial cell transcriptome much less significantly than the oral pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans perturbed the transcriptome, indicating that there was a greater degree of host adaptation by the commensal species (M. Handfield, J. J. Mans, G. Zheng, M. C. Lopez, S. Mao, A. Progulske-Fox, G. Narasimhan, H. V. Baker, and R. J. Lamont, Cell. Microbiol. >7:811-823, 2005). The biological pathways significantly impacted by F. nucleatum and S. gordonii included the mitogen-activated protein kinase (MAPK) and Toll-like receptor signaling pathways. Differential regulation of GADD45 and DUSP4, key components of the MAPK pathway, was confirmed at the protein level by Western blotting. Modulation of the MAPK pathway is likely to affect host cell proliferation and differentiation. In addition, both the MAPK and Toll-like receptor pathways ultimately converge on cytokine gene expression. An enzyme-linked immunosorbent assay of secreted interleukin-6 (IL-6) and IL-8 demonstrated that F. nucleatum induced production of these cytokines, whereas S. gordonii inhibited secretion from the epithelial cells. Stimulation of secretion of proinflammatory cytokines from epithelial cells may reflect the invasive phenotype of F. nucleatum and contribute to the greater pathogenic potential of F. nucleatum than of S. gordonii.
机译：利用转录谱分析和本体论工具，确定了口腔粘膜炎性链球菌和机会性粘液性融合菌共培养对牙龈上皮细胞生物学途径的影响。总体而言， F。核和 S。戈登氏菌对牙龈上皮细胞转录组的干扰远小于口腔病原体牙龈卟啉单胞菌和放线杆菌聚合酶对口腔转录组的干扰，表明宿主的程度更高常见物种的适应性（M. Handfield，JJ Mans，G。Zheng，MC Lopez，S。Mao，A。Progulske-Fox，G。Narasimhan，HV Baker和RJ Lamont，Cell.Microbiol。> 7： 811-823，2005）。生物途径受到 F的显着影响。核和 S。 gordonii 包括促分裂原活化蛋白激酶（MAPK）和Toll样受体信号通路。通过蛋白质印迹在蛋白质水平上证实了GADD45和DUSP4（MAPK途径的关键成分）的差异调节。 MAPK途径的调节可能会影响宿主细胞的增殖和分化。此外，MAPK和Toll样受体途径最终都收敛于细胞因子基因的表达。分泌的白介素6（IL-6）和IL-8的酶联免疫吸附试验表明 F。核诱导了这些细胞因子的产生，而 S。戈登氏菌抑制了上皮细胞的分泌。刺激上皮细胞分泌促炎细胞因子可能反映了 F的侵袭性表型。核并有助于 F的更大致病潜力。核比 S。戈多尼。

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