Epstein-Barr Virus Promotes the Production of Inflammatory Cytokines in Gingival Fibroblasts and RANKL-Induced Osteoclast Differentiation in RAW264.7 Cells.

Epstein-Barr Virus Promotes the Production of Inflammatory Cytokines in Gingival Fibroblasts and RANKL-Induced Osteoclast Differentiation in RAW264.7 Cells.
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DOI:
10.3390/ijms23020809
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发表时间:
2022-01-12
影响因子:
5.6
通讯作者:
Imai K
Imai K
中科院分区:
生物学2区
文献类型:
--
作者:
Yokoe S;Hasuike A;Watanabe N;Tanaka H;Karahashi H;Wakuda S;Takeichi O;Kawato T;Takai H;Ogata Y;Sato S;Imai K

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牙周炎是一种导致牙齿支撑组织破坏的炎症性疾病,是影响全球一半以上成年人口的主要公共卫生问题。最近,疱疹病毒家族的成员,如EB病毒(EBV),已被认为是参与牙周炎的病因,因为细菌活动本身并不能充分解释牙周炎的临床特征。然而,EBV在牙周炎病因中的作用尚不清楚。本研究旨在探讨灭活EBV对人牙龈成纤维细胞(HGFs)表达炎性细胞因子和诱导破骨细胞分化的影响。我们发现,极高水平的白细胞介素(IL)-6和IL-8诱导灭活EBV在复制依赖性的方式在HGF。当细胞用EBV处理时,HGF中IL-6和IL-8的水平高于用脂多糖和脂磷壁酸处理时。EBV可诱导IκBα降解、NF-κB转录和RAW264.7细胞向破骨细胞样细胞分化。这些发现表明,即使没有感染细胞,EBV也通过与口腔细胞或巨噬细胞谱系接触而促进炎性细胞因子的产生和破骨细胞的分化,导致牙周炎的发作和进展。
Periodontitis is an inflammatory condition that causes the destruction of the supporting tissues of teeth and is a major public health problem affecting more than half of the adult population worldwide. Recently, members of the herpes virus family, such as the Epstein–Barr virus (EBV), have been suggested to be involved in the etiology of periodontitis because bacterial activity alone does not adequately explain the clinical characteristics of periodontitis. However, the role of EBV in the etiology of periodontitis is unknown. This study aimed to examine the effect of inactivated EBV on the expression of inflammatory cytokines in human gingival fibroblasts (HGFs) and the induction of osteoclast differentiation. We found that extremely high levels of interleukin (IL)-6 and IL-8 were induced by inactivated EBV in a copy-dependent manner in HGFs. The levels of IL-6 and IL-8 in HGFs were higher when the cells were treated with EBV than when treated with lipopolysaccharide and lipoteichoic acid. EBV induced IκBα degradation, NF-κB transcription, and RAW264.7 cell differentiation into osteoclast-like cells. These findings suggest that even without infecting the cells, EBV contributes to inflammatory cytokine production and osteoclast differentiation by contact with oral cells or macrophage lineage, resulting in periodontitis onset and progression.
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