OBJECTIVES This study was established to investigate whether the chemokines CXCL1, CCL2, and CCL5 are produced in periodontal cells and tissues and, if so, whether their levels are regulated by microbial and/or mechanical signals. MATERIALS AND METHODS The chemokine expression and protein levels in gingival biopsies from patients with and without periodontitis were analyzed by RT-PCR and immunohistochemistry. The chemokines were also analyzed in gingival biopsies from rats subjected to experimental periodontitis and/or orthodontic tooth movement. Additionally, chemokine levels were determined in periodontal fibroblasts exposed to the periodontopathogen Fusobacterium nucleatum and mechanical forces by RT-PCR and ELISA. RESULTS Higher CXCL1, CCL2, and CCL5 levels were found in human and rat gingiva from sites of periodontitis as compared with periodontally healthy sites. In the rat experimental periodontitis model, the bacteria-induced upregulation of these chemokines was significantly counteracted by orthodontic forces. In vitro, F. nucleatum caused a significant upregulation of all chemokines at 1 day. When the cells were subjected simultaneously to F. nucleatum and mechanical forces, the upregulation of chemokines was significantly inhibited. The transcriptional findings were paralleled at protein level. CONCLUSIONS This study provides original evidence in vitro and in vivo that the chemokines CXCL1, CCL2, and CCL5 are regulated by both microbial and mechanical signals in periodontal cells and tissues. Furthermore, our study revealed that biomechanical forces can counteract the stimulatory actions of F. nucleatum on these chemokines. CLINICAL RELEVANCE Mechanical loading might aggravate periodontal infection by compromising the recruitment of immunoinflammatory cells.

中文翻译：

---

牙周细胞和组织中微生物和生物力学信号对CXCL1，CCL2和CCL5的调节-体外和体内研究。

目的建立本研究以调查在牙周细胞和组织中是否产生趋化因子CXCL1，CCL2和CCL5，如果是，则其水平是否受微生物和/或机械信号调节。材料与方法采用RT-PCR和免疫组化技术分析有牙周炎和无牙周炎的患者牙龈活检组织中的趋化因子表达和蛋白水平。还从经受实验性牙周炎和/或正畸牙齿运动的大鼠的牙龈活检中分析了趋化因子。另外，通过RT-PCR和ELISA测定暴露于牙周病原体核杆菌中的牙周成纤维细胞中的趋化因子水平和机械力。结果CXCL1，CCL2，与牙周健康部位相比，在牙周炎部位的人和大鼠齿龈中发现了CCL5和CCL5水平。在大鼠实验性牙周炎模型中，正畸力明显抵消了细菌诱导的这些趋化因子的上调。在体外，在第1天时，核仁引起所有趋化因子的显着上调。当细胞同时受到细胞核和机械力作用时，趋化因子的上调被显着抑制。转录结果在蛋白质水平上是平行的。结论这项研究提供了体外和体内趋化因子CXCL1，CCL2和CCL5受牙周细胞和组织中微生物和机械信号调节的原始证据。此外，我们的研究表明，生物力学力可以抵消核镰刀菌对这些趋化因子的刺激作用。临床意义机械负荷可能通过损害免疫炎症细胞的募集而加重牙周感染。