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Regulation of Periodontal Ligament Cell Functions by Interleukin-1β

机译：白细胞介素-1β对牙周膜细胞功能的调节

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Periodontal ligament (PDL) cells maintain the attachment of the tooth to alveolar bone. These cells reside at a site in which they are challenged frequently by bacterial products and proinflammatory cytokines, such as interleukin-1β (IL-1β), during infections. In our initial studies we observed that IL-1β down-regulates the osteoblast-like characteristics of PDL cells in vitro. Therefore, we examined the functional significance of the loss of the PDL cell’s osteoblast-like characteristics during inflammation. In this report we show that, during inflammation, IL-1β can modulate the phenotypic characteristics of PDL cells to a more functionally significant lipopolysaccharide (LPS)-responsive phenotype. In a healthy periodontium PDL cells exhibit an osteoblast-like phenotype and are unresponsive to gram-negative bacterial LPS. Treatment of PDL cells with IL-1β inhibits the expression of their osteoblast-like characteristics, as assessed by the failure to express transforming growth factor β1 (TGF-β1) and proteins associated with mineralization, such as alkaline phosphatase and osteocalcin. As a consequence of this IL-1β-induced phenotypic change, PDL cells become responsive to LPS and synthesize proinflammatory cytokines. The IL-1β-induced phenotypic changes in PDL cells were transient, as removal of IL-1β from PDL cell cultures resulted in reacquisition of their osteoblast-like characteristics and lack of LPS responsiveness. The IL-1β-induced phenotypic changes occurred at concentrations that are frequently observed in tissue exudates during periodontal inflammation (0.05 to 5 ng/ml). The results suggest that, during inflammation in vivo, IL-1β may modulate PDL cell functions, allowing PDL cells to participate directly in the disease process by assuming LPS responsiveness at the expense of their normal structural properties and functions.
机译：牙周膜（PDL）细胞维持牙齿与牙槽骨的附着。这些细胞位于感染期间细菌产品和促炎细胞因子（例如白介素-1β（IL-1β））经常攻击的位置。在我们的初步研究中，我们观察到IL-1β在体外下调PDL细胞的成骨样特征。因此，我们研究了炎症过程中PDL细胞成骨样特征丧失的功能意义。在此报告中，我们表明，在炎症过程中，IL-1β可以将PDL细胞的表型特征调节为功能上更重要的脂多糖（LPS）响应型。在健康的牙周膜中，PDL细胞表现出成骨细胞样表型，并且对革兰氏阴性细菌LPS无反应。用IL-1β处理PDL细胞会抑制其成骨细胞样特征的表达，这通过无法表达转化生长因子β1（TGF-β1）和与矿化相关的蛋白质（例如碱性磷酸酶和骨钙素）来评估。这种IL-1β诱导的表型改变的结果是，PDL细胞对LPS产生反应并合成促炎细胞因子。 IL-1β诱导的PDL细胞表型改变是短暂的，因为从PDL细胞培养物中去除IL-1β会导致其成骨样特征的重新获得和LPS反应性的缺乏。 IL-1β诱导的表型变化发生在牙周炎症期间组织渗出液中经常观察到的浓度（0.05至5 ng / ml）。结果表明，在体内炎症过程中，IL-1β可能会调节PDL细胞功能，从而通过假设LPS反应性而牺牲其正常的结构特性和功能，从而使PDL细胞直接参与疾病过程。

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