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.

项目总结/摘要 牙周病（PD）影响了大约50%的世界人口。微生物生态失调和牙龈 炎症在PD中是公认。然而，饮食对这些参数的作用是最低限度的探索。 PD发病率的增加与西方饮食的采用相一致，西方饮食的特点是消耗 高度加工的精制谷物谷物加工改变了谷物的营养和结构特性， 去除外麸层以分离内部富含淀粉的组分。这破坏了谷物的完整性 结构，从而增加淀粉的生物利用度和更精细的谷物质地。精粮消费是 与PD发病率增加有关。然而，细化晶粒增加PD的机制 发病率尚未调查。消化在口服阶段通过唾液淀粉酶的淀粉水解开始， 通过咀嚼进行机械消化。通过淀粉， 由唾液淀粉酶水解。糖利用率的增加改变了微生物的碳水化合物代谢， 驱动了牙牙龈生物膜群落内的微生物生态失调。牙龈表面提供了一个 成熟微生物生物膜形成的机会。过量的生物膜形成驱动生态失调， 定植增加了牙周病原体在群落中的代表性。因此，机械 需要清创术来破坏生物膜的形成。增加饮食质地已被证明可以减少生物膜 积累此外，增加咀嚼力的硬饮食诱导保护性炎症反应 在牙龈组织中，与牙龈作为生理屏障的作用一致。随着谷物加工的增加 淀粉生物利用度和对唾液淀粉酶的敏感性，这可能增加糖的可用性， 口腔中的细菌，并鼓励生态失调。此外，由于谷物加工破坏了 当牙齿的颗粒结构发生变化时，这种变化可能会降低咀嚼力，从而促进过量的微生物生长。 定植并降低牙龈屏障功能。因此，我假设加工过的谷物会导致PD 通过促进微生物生态失调和/或通过经由牙龈屏障功能降低来促进牙龈疾病的进展。 口腔内的局部影响。这个建议将通过两个具体目标来解决我的假设：1） 确定加工谷物对体外多物种牙龈生物膜形成的影响，以及2） 确定加工谷物对牙龈微生物组、牙周免疫反应和 体内牙龈屏障功能。这些目标将利用体外和体内模型的组合来实现 为了概括牙龈微生物组和牙周免疫的变化， 粮食消费。这项研究的结果将提高对饮食在PD中作用的理解 进展，并将创造新的治疗应用，利用口服 微生物组用于预防PD发作和进展。