Nuclear factor-kappaB p50 subunits in chronic periodontitis and Porphyromonas gingivalis lipopolysaccharide-pulsed dendritic cells.
Nuclear factor-kappaB p50 subunits in chronic periodontitis and Porphyromonas gingivalis lipopolysaccharide-pulsed dendritic cells.
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DOI：
10.1111/j.1749-6632.2009.05247.x
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发表时间：
2010-03
影响因子：
5.2
通讯作者：
Cutler CW
中科院分区：
文献类型：
--
作者：
Jotwani R;Moonga BS;Gupta S;Cutler CW
The pathogenesis of a number of chronic inflammatory diseases has been linked to dysregulated functioning of nuclear transcription factor NF-κB. In the present study, we examine NF-κB activation in human oral mucosal tissues of chronic periodontitis (CP) patients. We find through EMSA and DNA binding ELISAs that there are elevated levels of transcriptionally repressive p50 subunits and increased p50:p65 ratio in CP tissues compared to healthy controls. Because P. gingivalis has been recognized to be a causal factor in CP, we used P. gingivalis LPS for in vitro studies with monocyte-derived dendritic cells (MoDCs). We find that P. gingivalis LPS, unlike E. coli LPS, induces an increased p50:p65 ratio in MoDCs. Using blocking antibodies, we observed that while both TLR2 and TLR4 are required for MoDC maturation by P. gingivalis LPS, only TLR4 signaling is sufficient to induce cytokine secretion. Our results suggest that increased levels of transcriptionally repressive p50 may be characteristic of CP and might be a result of suboptimal NF-κB activation and dendritic cell maturation by P. gingivalis, a bacterium implicated in CP.
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