Porphyromonas gingivalis Peptidyl Arginine Deiminase Can Modulate Neutrophil Activity via Infection of Human Dental Stem Cells.

Porphyromonas gingivalis Peptidyl Arginine Deiminase Can Modulate Neutrophil Activity via Infection of Human Dental Stem Cells.
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牙龈卟啉单胞菌肽基精氨酸脱亚胺酶可以通过感染人牙干细胞来调节中性粒细胞活性。

DOI:
10.1159/000489020
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发表时间:
2018
影响因子:
5.3
通讯作者:
Kreikemeyer,Bernd
Kreikemeyer,Bernd
中科院分区:
医学2区
文献类型:
--
作者:
Kriebel,Katja;Hieke,Cathleen;Engelmann,Robby;Potempa,Jan;Müller-Hilke,Brigitte;Lang,Hermann;Kreikemeyer,Bernd

文献摘要

相似文献

牙周炎(Periodontitis,PD)是一种常见的慢性炎症性疾病,牙龈卟啉单胞菌(Porphyromonasgingivalisis)与PD相关,可通过P途径使宿主蛋白质发生瓜氨酸化。牙龈炎肽酰精氨酸脱亚胺酶(PPAD)。在这里,我们假设感染人牙囊干细胞(hDFSCs)与P。牙龈炎以及随后与中性粒细胞的相互作用将改变中性粒细胞的表型。为了验证这一假设,我们建立并分析了中性粒细胞和用P.牙龈炎应用促分裂原活化途径阻断剂来深入了解感染后的干细胞信号传导。幼稚hDFSC不影响中性粒细胞表型。但感染P.牙龈炎抑制中性粒细胞的存活并增加其迁移。这些表型变化依赖于直接的细胞接触和PPAD的表达。牙龈炎致敏hDFSC中的活性JNK和ERK途径对于中性粒细胞的表型变化是必不可少的。总的来说,我们的结果证实,P。牙龈炎修饰hDFSC,从而引起免疫失衡。
Periodontitis (PD) is a widespread chronic inflammatory disease in the human population.Porphyromonas gingivalisis associated with PD and can citrullinate host proteins viaP. gingivalispeptidyl arginine deiminase (PPAD). Here, we hypothesized that infection of human dental follicle stem cells (hDFSCs) withP. gingivalisand subsequent interaction with neutrophils will alter the neutrophil phenotype. To test this hypothesis, we established and analyzed a triple-culture system of neutrophils and hDFSCs primed withP. gingivalis. Mitogen-activated pathway blocking reagents were applied to gain insight into stem cell signaling after infection. Naïve hDFSCs do not influence the neutrophil phenotype. However, infection of hDFSCs withP. gingivalisprolongs the survival of neutrophils and increases their migration. These phenotypic changes depend on direct cellular contacts and PPAD expression byP. gingivalis. Active JNK and ERK pathways in primed hDFSCs are essential for the phenotypic changes in neutrophils. Collectively, our results confirm thatP. gingivalismodifies hDFSCs, thereby causing an immune imbalance.