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/文摘