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; 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 牙周疾病（PD）影响了大约50％的世界人口。微生物营养不良和牙龈 炎症在PD中得到了很好的认识。但是，饮食对这些参数的作用是最少的。 PD发病率的增加与采用西方饮食相吻合，其特征是消费 高度加工的精制谷物。谷物加工通过 去除外麸皮层以隔离内部淀粉富的成分。这破坏了谷物的完整性 结构，导致淀粉的生物利用度增加和较细的谷物质地。精制的谷物消耗是 与PD的发生率增加有关。但是，精制谷物增加PD的机制 发病率没有探索。消化通过唾液淀粉酶和 通过咀嚼的机械消化。糖可通过淀粉可用于口腔中的细菌 唾液淀粉酶水解。糖精的可用性增加会改变微生物碳水化合物代谢， 在牙本质生物膜群落中驱动微生物营养不良。牙本质表面提供 成熟微生物生物膜形成的机会。过多的生物膜形成驱动失调作为继承 殖民化增加了社区内牙周病原体的表示。因此，机械 需要清创术来破坏生物膜的形成。饮食质地的增加已显示可降低生物膜 积累。此外，硬饮食增加的咀嚼力会引起保护性炎症反应 在牙龈组织中，与牙龈作为生理障碍的作用一致。随着谷物处理的增加 淀粉生物利用度及其对唾液淀粉酶的敏感性，这可能会使糖的供应性增加到 口腔中的细菌并鼓励营养不良。此外，随着谷物处理破坏 谷物结构，这种变化可能会减少咀嚼力，从而鼓励过量的微生物 定植并降低牙龈屏障功能。因此，我假设加工后的谷物会诱导PD 通过促进微生物营养不良和/或通过减少牙龈屏障功能来进展 口腔内的局部影响。该提议将通过两个具体目的解决我的假设：1） 确定加工晶粒对体外牙科生物膜的发展的影响，以及2） 确定加工晶粒对牙本质微生物组，牙周免疫反应和 牙龈屏障功能在体内。利用体外模型的组合，将实现这些目标 响应于处理 消耗谷物。这项调查的结果将提高人们对饮食在PD中的作用的理解 进展并将为开发新型治疗应用而创造途径 用于预防PD发作和进展的微生物组。