Cytolethal distending toxin upregulates RANKL expression in Jurkat T-cells
Cytolethal distending toxin upregulates RANKL expression in Jurkat T-cells
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DOI：
10.1111/j.1600-0463.2008.01017.x
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发表时间：
2008-06-01
期刊：
影响因子：
2.8
通讯作者：
Johansson, Anders
中科院分区：
文献类型：
--
作者：
Belibasakis, Georgios N.;Brage, Monica;Johansson, Anders
胞毒膨胀毒素是一种由许多革兰氏阴性菌产生的细菌外毒素，可引起宿主细胞生长停滞和形态改变。在这些物种中，杜氏嗜血杆菌是软下疳的病原，而牙周病原体放线菌聚集菌与局部侵袭性牙周炎密切相关。CDT诱导牙周成纤维细胞中nf - κ B配体受体激活因子（receptor activator of nf - κ B ligand， RANKL）的表达。t细胞积极参与局部炎症引起的骨破坏，包括牙周炎。本研究的目的是研究纯化CDT对Jurkat t细胞系中RANKL及其诱饵受体骨保护素（OPG）表达的影响。实时荧光定量PCR结果显示，100pg /ml纯化的h . ducreyi CDT暴露24 h后，RANKL mRNA表达上调2.2倍。通过ELISA测定，RANKL蛋白释放增加了2.0倍，证实了这种增加。本实验系统未检测到OPG。总之，CDT增强了t细胞中RANKL的表达，表明这些细胞是毒素的潜在靶点，并加强了这种毒力因子与局部骨吸收相关机制之间的潜在联系。
Cytolethal distending toxin, a bacterial exotoxin produced by a number of Gram-negative species, causes growth arrest and morphological alterations in host cells. Among these species are Haemophilus ducreyi, the etiological agent of chancroid, and the periodontal pathogen Aggregatibacter actinomycetemcomitans, highly implicated in localized aggressive periodontitis. CDT induces receptor activator of NF-kappa B ligand (RANKL) expression in periodontal fibroblasts, the key bone-resorbing cytokine. T-cells are actively involved in localized inflammation-induced bone destruction, including periodontitis. The aim of this study was to investigate the effects of purified CDT on the expression of RANKL and its decoy receptor osteoprotegerin (OPG), in the Jurkat T-cell line. Quantitative real-time PCR indicated that 100 pg/ml of purified H. ducreyi CDT upregulated RANKL mRNA expression by 2.2-fold, after 24 h of exposure. This increase was corroborated by a 2.0-fold increase in RANKL protein release, as determined by ELISA. OPG was not detected in this experimental system. In conclusion, CDT enhances RANKL expression in T-cells, denoting that these cells are a potential target for the toxin and strengthening the potential link between this virulence factor and mechanisms associated with localized bone resorption.