The Effect of Processed Grain Consumption on the Dentogingival Microbiome and Host Response in Periodontal Disease

加工谷物消费对牙周病牙龈微生物组和宿主反应的影响

• 批准号: 10442422
• 负责人: Lea Maryam Sedghi
• 金额: $ 5.26万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2021
• 资助国家: 美国
• 起止时间: 2021-07-01 至 2025-06-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10442422
• 关键词: 16S ribosomal RNA sequencing; Actinomyces; Address; Adoption; Affect; Alveolar Bone Loss; Amylases; Automobile Driving; Bacteria; Biological Availability; Bite Force; Carbohydrates; Cells; Communities; Complementary DNA; Consumption; Data; Debridement; Development; Diet; Digestion; Disease; Disease Progression; E-Cadherin; Epithelial Cells; Excision; Flow Cytometry; Fluorescent in Situ Hybridization; Food; Forsythia; Fusobacterium nucleatum; Gene Expression; Genetic Transcription; Gingiva; Grain; Growth; Harvest; Hydrolysis; Immune; Immune response; Immunity; Immunohistochemistry; In Vitro; Incidence; Infection; Inflammation; Inflammatory Response; Investigation; Mastication; Mechanics; Microbial Biofilms; Microfluidics; Modeling; Mus; Nutritional; Onset of illness; Oral; Oral cavity; Outcome; Periodontal Diseases; Periodontal Ligament; Phase; Physiological; Population; Porphyromonas gingivalis; Predisposition; Prevention; Process; Property; RNA; Roentgen Rays; Role; Salivary; Site; Soft Diet; Standardization; Starch; Streptococcus gordonii; Streptococcus sanguis; Structure; Surface; System; Texture; Tissues; Transcript; Transmission Electron Microscopy; Treponema denticola; Virulence; Western Blotting; Wheat; base; beta catenin; carbohydrate metabolism; dysbiosis; improved; in vivo; in vivo Model; light microscopy; mandible/maxilla; microCT; microbial; microbial colonization; microbiome; novel strategies; novel therapeutic intervention; novel therapeutics; oral microbial community; oral microbiome; particle; pathogen; periodontopathogen; polymicrobial biofilm; response; tomography; transcriptome sequencing; western diet

PROJECT SUMMARY/ABSTRACT Periodontal disease (PD) affects approximately 50% of the world population. Microbial dysbiosis and gingival inflammation are well-recognized in PD. However, the role of diet on these parameters is minimally explored. Increased PD incidence coincides with the adoption of the western diet that is characterized by consumption of highly processed, refined grains. Grain processing alters both nutritional and structural properties of grains via removal of the outer bran layer to isolate inner starch-rich components. This disrupts the integrity of the grain structure, resulting in increased starch bioavailability and finer grain texture. Refined grain consumption is associated with increased incidence of PD. However, the mechanisms by which refined grains increase PD incidence are unexplored. Digestion commences in the oral phase via starch hydrolysis by salivary amylase and mechanical digestion by mastication. Saccharides are made available to bacteria in the oral cavity via starch hydrolysis by salivary amylase. Increased saccharide availability alters microbial carbohydrate metabolism, driving microbial dysbiosis within dentogingival biofilm communities. Dentogingival surfaces provide an opportunity for mature microbial biofilm formation. Excess biofilm formation drives dysbiosis as successional colonization increases the representation of periodontal pathogens within the community. As such, mechanical debridement is required to disrupt biofilm formation. Increased diet texture has been shown to decrease biofilm accumulation. Moreover, increased masticatory forces by hard diets induce a protective inflammatory response in gingival tissues, consistent with the role of the gingiva as a physiological barrier. As grain processing increases starch bioavailability and its susceptibility to salivary amylase, this may increase saccharide availability to bacteria in the oral cavity and encourage dysbiosis. Moreover, as grain processing disrupts the integrity of the grain structure, such changes may reduce masticatory forces and thereby encourage excess microbial colonization and reduce gingival barrier function. Therefore, I hypothesize that processed grains induce PD progression by promoting microbial dysbiosis and/or by conferring reduced gingival barrier function via local influences within the oral cavity. This proposal will address my hypothesis via two specific aims: 1) Determine the impact of processed grains on development of multispecies dentogingival biofilms in vitro, and 2) Determine the impact of processed grains on the dentogingival microbiome, periodontal immune response, and gingival barrier function in vivo. These aims will be achieved utilizing a combination of in vitro and in vivo models to recapitulate changes in the dentogingival microbiome and periodontal immunity in response to processed grain consumption. Outcomes from this investigation will improve the understanding of the role of diet in PD progression and will create avenues for the development of novel therapeutic applications that leverage the oral microbiome for prevention of PD onset and progression.

项目摘要/摘要 牙周病(PD)影响约50%的世界人口。微生物代谢失调与牙龈 炎症在帕金森病患者中是公认的。然而，饮食对这些参数的作用是最低限度的探索。 帕金森病发病率的增加与西方饮食的采用不谋而合，西方饮食的特点是摄入 经过高度加工的精制谷物。谷物加工通过以下途径改变谷物的营养和结构特性 去除外层麸皮以分离内部富含淀粉的成分。这破坏了谷物的完整性 结构，从而提高了淀粉的生物利用率和更好的谷物质地。精细化粮食消费是 与帕金森病发病率的增加有关。然而，细化颗粒增加PD的机制 发病率是未被研究的。消化开始于口腔阶段，通过唾液淀粉酶的淀粉水解酶和 通过咀嚼进行机械消化。口腔中的细菌可以通过淀粉获得糖类。 唾液淀粉酶的水解酶。糖类利用率的增加改变了微生物的碳水化合物代谢， 推动牙龈生物膜群落内的微生物生态失调。牙龈表面提供了一种 成熟的微生物生物膜形成的机会。过度的生物被膜形成推动了生物多样性的演替 定居增加了牙周病原体在社区中的代表性。因此，机械的 需要清创以破坏生物膜的形成。研究表明，饮食结构的增加会减少生物膜 积累。此外，硬质饮食增加的咀嚼力量会引起保护性炎症反应。 在牙龈组织中，符合牙周膜作为生理屏障的作用。随着粮食加工的增加 淀粉的生物利用率及其对唾液淀粉酶的敏感性，这可能会增加糖的利用率 口腔中的细菌，并鼓励生态失调。此外，由于谷物加工破坏了 颗粒结构，这种变化可能会减少咀嚼力量，从而鼓励过多的微生物 具有定植和减少牙龈屏障的作用。因此，我假设加工过的谷物会诱发帕金森病 促进微生物失调和/或通过以下途径降低牙龈屏障功能的进展 口腔内的局部影响。这项提议将通过两个具体目标解决我的假设：1) 测定加工颗粒对体外培养的多种牙龈生物膜形成的影响，以及2) 确定加工颗粒对牙周微生物群、牙周免疫反应和 牙龈屏障功能的体内研究。这些目标将利用体外和体内模型的组合来实现 概述了牙周微生物群和牙周免疫在处理后的变化 粮食消费。这项研究的结果将提高对饮食在帕金森病中的作用的理解 并将为开发利用口服的新的治疗应用创造途径 微生物组预防帕金森病的发生和发展。