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抗菌肽P-113-DPS抑制……的致龋毒力 。 (原文此处不完整,缺少具体被抑制致龋毒力的对象)

Antimicrobial Peptide P-113-DPS Suppresses the Cariogenic Virulence of .

作者信息

Liu Qing, Zhou Li, Peng Simin, Li Quan Li, Wong Hai Ming

机构信息

Paediatric Dentistry and Orthodontics, Faculty of Dentistry, The University of Hong Kong, Hong Kong SAR 999077, China.

Institute of Oral Science, Department of Stomatology, Longgang Otorhinolaryngology Hospital, No. 3004L Longgang Avenue, Shenzhen 518172, China.

出版信息

ACS Appl Bio Mater. 2025 Jun 16;8(6):4973-4980. doi: 10.1021/acsabm.5c00314. Epub 2025 Jun 1.

Abstract

Dental caries is a widespread and contagious chronic infectious condition. As the principal cariogenic bacterium involved in dental caries, () possesses cariogenicity-related properties, including acidogenicity, aciduricity, and exopolysaccharide (EPS) synthesis. Our previously designed peptide, P-113-DPS, has demonstrated antibacterial effects on ; however, its detailed impact on its cariogenic virulence factors remains unclear. This study focused on assessing changes in these factors following treatment with P-113-DPS. Furthermore, it aimed to investigate alterations in virulence-associated gene expression . The basic viability of after P-113-DPS treatment was evaluated using a growth curve assay and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide staining assay. Acidogenicity was assessed through monitoring pH drop and lactate dehydrogenase activity, while aciduricity was evaluated through measuring survival rates in a lethal acidic environment. Additionally, EPS synthesis was analyzed using the anthrone sulfuric acid method, and structural observations were performed with confocal laser scanning and scanning electron microscopy. Finally, the changes in gene expression were examined utilizing quantitative real-time PCR (qPCR). P-113-DPS inhibited the growth and cell viability of . Treatment with P-113-DPS resulted in decreased acidogenicity and aciduricity, evidenced by reduced acid production and survival rates at pH 5.0. Additionally, P-113-DPS suppressed the biofilm formation and EPS synthesis. Moreover, qPCR analysis revealed that P-113-DPS downregulated the expression of virulence-associated genes. In conclusion, P-113-DPS exhibited strong antimicrobial properties and effectively suppressed the cariogenic virulence traits of by downregulating virulence-associated genes, highlighting its promising anticaries potential.

摘要

龋齿是一种广泛传播且具有传染性的慢性感染性疾病。作为参与龋齿形成的主要致龋菌,(此处原文缺失具体细菌名称)具有与致龋性相关的特性,包括产酸性、耐酸性和胞外多糖(EPS)合成能力。我们之前设计的肽P - 113 - DPS已显示出对(此处原文缺失具体细菌名称)的抗菌作用;然而,其对致龋毒力因子的具体影响仍不清楚。本研究着重评估P - 113 - DPS处理后这些因子的变化。此外,旨在研究毒力相关基因表达的改变。使用生长曲线测定法和3 -(4,5 - 二甲基噻唑 - 2 - 基)- 2,5 - 二苯基四氮唑溴盐染色测定法评估P - 113 - DPS处理后(此处原文缺失具体细菌名称)的基本活力。通过监测pH下降和乳酸脱氢酶活性评估产酸性,而通过测量在致死性酸性环境中的存活率评估耐酸性。另外,使用蒽酮硫酸法分析EPS合成,并通过共聚焦激光扫描和扫描电子显微镜进行结构观察。最后,利用定量实时PCR(qPCR)检测基因表达的变化。P - 113 - DPS抑制了(此处原文缺失具体细菌名称)的生长和细胞活力。P - 113 - DPS处理导致产酸性和耐酸性降低,表现为在pH 5.0时酸产生减少和存活率降低。此外,P - 113 - DPS抑制生物膜形成和EPS合成。而且,qPCR分析显示P - 113 - DPS下调了(此处原文缺失具体细菌名称)毒力相关基因的表达。总之,P - 113 - DPS表现出强大的抗菌特性,并通过下调毒力相关基因有效抑制了(此处原文缺失具体细菌名称)的致龋毒力特征,突出了其有前景的防龋潜力。

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