Kozak Małgorzata, Poniewierska-Baran Agata, Czerewaty Michał, Łuczkowska Karolina, Safranow Krzysztof, Mazurek-Mochol Małgorzata, Machaliński Bogusław, Pawlik Andrzej
Department of Dental Prosthetics, Pomeranian Medical University, 70-111 Szczecin, Poland.
Institute of Biology, University of Szczecin, 71-412 Szczecin, Poland.
Biology (Basel). 2025 Mar 21;14(4):321. doi: 10.3390/biology14040321.
Periodontitis is a disease caused by a bacterial infection that causes chronic inflammation. The pathogenesis of periodontitis is mediated by several mediators, including chemokines, cytokines, metalloproteinases, and adipokines. Adiponectin is an adipokine that influences several metabolic processes and numerous immunological processes. In this study, we investigated the effect of adiponectin on the expression in the periodontal ligament of selected cytokines involved in the pathogenesis of periodontitis. Human periodontal ligament cells (hPDLCs) were stimulated with adiponectin and then analyzed for expression (TNF-α, IL-1, IL-6, IL-8, IL-10, IL-17, and IL-18) in cell cultures at the mRNA level and in supernatants at the protein level. The samples were analyzed after 12, 24, and 48 h of adiponectin stimulation. We found no significant effect of adipokine on TNF-α gene expression after 12, 24, and 48 h of stimulation. For IL-1, a statistically significant increase in gene expression was found after 12 h of adiponectin stimulation, while the differences were not statistically significant after 24 and 48 h. Adiponectin caused a statistically significant increase in gene expression after 12, 24, and 48 h of stimulation. Stimulating periodontal ligament cells with adiponectin significantly increased TNF-α, IL-6, and IL-8 protein levels in supernatants after 12, 24, and 48 h. The levels of IL-1 were statistically significantly increased after 12 and 24 h of adiponectin stimulation. There was no statistically significant effect of adiponectin on IL-10, IL-17, and IL-18 levels. The results of our study suggest that adiponectin may significantly increase the expression of selected cytokines in periodontal ligament cells.
牙周炎是一种由细菌感染引起的导致慢性炎症的疾病。牙周炎的发病机制由多种介质介导，包括趋化因子、细胞因子、金属蛋白酶和脂肪因子。脂联素是一种影响多种代谢过程和众多免疫过程的脂肪因子。在本研究中，我们调查了脂联素对牙周炎发病机制中涉及的选定细胞因子在牙周膜中表达的影响。用人牙周膜细胞（hPDLCs）进行脂联素刺激，然后在细胞培养物中分析其在mRNA水平的表达（TNF-α、IL-1、IL-6、IL-8、IL-10、IL-17和IL-18）以及在蛋白质水平的上清液中的表达。在脂联素刺激12、24和48小时后对样本进行分析。我们发现，在刺激12、24和48小时后，脂肪因子对TNF-α基因表达没有显著影响。对于IL-1，脂联素刺激12小时后基因表达有统计学意义的增加，而在24和48小时后差异无统计学意义。脂联素在刺激12、24和48小时后导致基因表达有统计学意义的增加。用脂联素刺激牙周膜细胞在12、24和48小时后显著增加了上清液中TNF-α、IL-6和IL-8的蛋白质水平。脂联素刺激12和24小时后IL-1水平有统计学意义的显著增加。脂联素对IL-10、IL-17和IL-18水平没有统计学意义的影响。我们的研究结果表明，脂联素可能显著增加牙周膜细胞中选定细胞因子的表达。
