Gingival epithelial cell transcriptional responses to commensal and opportunistic oral microbial species
Gingival epithelial cell transcriptional responses to commensal and opportunistic oral microbial species
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DOI：
10.1128/iai.01957-06
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发表时间：
2007-05-01
影响因子：
3.1
通讯作者：
Lamont, Richard J.
中科院分区：
文献类型：
--
作者：
Hasegawa, Yoshiaki;Mans, Jeffrey J.;Lamont, Richard J.
利用转录谱和本体论工具来定义牙龈上皮细胞的生物学途径，牙龈上皮细胞通过与口腔牙龈链球菌和机会性牙龈具核梭杆菌共培养来调节。总体而言，F。nucleatum和S. gordonii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伴放线菌聚集杆菌对转录组的干扰，表明牙龈菌属物种（M. Handfield，J. J. Mans，G. Zheng，M.，中国科学院昆虫研究所所长。C.洛佩斯，S. Mao，毛氏A. Progulske-Fox，G. Narasimhan，H. V. Baker和R. J.拉蒙，细胞。Microbiol. 7：811-823，2005）。F. nucleatum和S. gordonii的信号通路包括丝裂原活化蛋白激酶（MAPK）和Toll样受体信号通路。通过蛋白质印迹法在蛋白质水平证实了MAPK途径的关键组分GADD 45和DUSP 4的差异调节。MAPK通路的调节可能影响宿主细胞增殖和分化。此外，MAPK和Toll样受体途径最终都集中在细胞因子基因表达上。用酶联免疫吸附法检测F. nucleatum诱导这些细胞因子的产生，而S. Gordonii抑制上皮细胞的分泌。刺激上皮细胞分泌促炎细胞因子可能反映了F. nucleatum，并有助于更大的致病潜力的F。nucleatum比S. gordonii。
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.