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工程化唾液肽可减少致龋生物膜引发的牙釉质脱矿。

Engineered Salivary Peptides Reduce Enamel Demineralization Provoked by Cariogenic Biofilm.

作者信息

Marin Lina Maria, Xiao Yizhi, Cury Jaime Aparecido, Siqueira Walter Luiz

机构信息

College of Dentistry, University of Saskatchewan, Saskatoon, SK S7N 5E4, Canada.

Schulich School of Dentistry, The University of Western Ontario, London, ON N6A 5C1, Canada.

出版信息

Microorganisms. 2022 Mar 30;10(4):742. doi: 10.3390/microorganisms10040742.

Abstract

Engineering of the acquired enamel pellicle using salivary peptides has been shown to be a promising anticaries strategy. However, the mechanisms by which these peptides protect teeth against tooth decay are not fully understood. In this study, we evaluated the effect of the engineered salivary peptides DR9-DR9 and DR9-RR14 on enamel demineralization in two experimental conditions: (1) adsorbed onto the enamel surface forming the AEP, and (2) forming the AEP combined with their use to treat the biofilms 2×/day, using a validated cariogenic Streptococcus mutans in vitro biofilm model. Biofilms were grown for 144 h on enamel slabs and then collected to determine the bacterial viability (CFU/biofilm) and biofilm mass (mg protein/biofilm), and to extract cellular/extracellular proteins, which were characterized by mass spectrometry. The culture medium was changed 2×/day to fresh medium, and pH (indicator of biofilm acidogenicity) and calcium concentration (indicator of demineralization) was determined in used medium. DR9-RR14 peptide significantly reduced enamel demineralization (p < 0.0001) in both experimental conditions. However, this peptide did not have a significant effect on biofilm biomass (p > 0.05) nor did it modulate the expression of cellular and extracellular bacterial proteins involved in biofilm cariogenicity. These findings suggest that DR9-RR14 may control caries development mainly by a physicochemical mechanism.

摘要

利用唾液肽构建获得性釉质 pellicle 已被证明是一种有前景的防龋策略。然而,这些肽保护牙齿免受龋齿侵害的机制尚未完全明确。在本研究中,我们在两种实验条件下评估了工程化唾液肽 DR9 - DR9 和 DR9 - RR14 对釉质脱矿的影响:(1)吸附在釉质表面形成获得性釉质 pellicle;(2)形成获得性釉质 pellicle 并结合每天两次使用它们来处理生物膜,使用经过验证的变形链球菌体外生物膜模型。生物膜在釉质块上生长 144 小时,然后收集以确定细菌活力(CFU/生物膜)和生物膜质量(mg 蛋白质/生物膜),并提取细胞内/外蛋白质,通过质谱对其进行表征。每天两次将培养基更换为新鲜培养基,并测定使用过的培养基中的 pH(生物膜产酸性指标)和钙浓度(脱矿指标)。在两种实验条件下,DR9 - RR14 肽均显著降低了釉质脱矿(p < 0.0001)。然而,该肽对生物膜生物量没有显著影响(p > 0.05),也未调节参与生物膜致龋性的细胞内和细胞外细菌蛋白质的表达。这些发现表明,DR9 - RR14 可能主要通过物理化学机制控制龋齿的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd10/9032980/b61c3088822c/microorganisms-10-00742-g001.jpg

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