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PPARs and periodontal disease

PPAR 和牙周病

基本信息

批准号：
8968210
负责人：
FRANK C GIBSON
金额：
$ 26.1万
依托单位：
BOSTON MEDICAL CENTER
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-07-01 至 2017-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8968210
关键词：
Agonist Animal Model Area Bacterial Infections Calculi Cell Line Cell model Cells Chronic Clinical Research Clinical Treatment Complement Receptor Complex Coupled Data Debridement Development Elements Epithelial Cells Forsythia Future Gene Expression Gingiva Human Human Cell Line Immune Immune response Immunoglobulin G In Vitro Infection Inflammation Inflammatory Inflammatory Response Investigation Knowledge Ligature Measurement Measures Modality Modeling Mus Nuclear Hormone Receptors Operative Surgical Procedures Oral Outcome PPAR gamma Pathogenesis Pathology Patients Periodontal Diseases Peroxisome Proliferator-Activated Receptors Play Porphyromonas gingivalis Production Publishing Receptor Gene Recovery Role Testing Therapeutic Therapeutic Uses Tissues Treponema denticola Tumor Necrosis Factor-alpha antimicrobial base bone loss cytokine human tissue in vivo Model macrophage mouse model new therapeutic target novel novel strategies oral infection pathogen prevent public health relevance response scaling and root planing targeted treatment therapeutic target translational study treatment strategy

项目摘要

DESCRIPTION (provided by applicant): Porphyromonas gingivalis (Pg) is a keystone periodontal pathogen. Controlling chronic inflammation elicited by periodontal pathogens is thought central to mitigating soft and hard tissue destruction that characterizes periodontal disease (PD). Clinical treatment of patients with moderate to severe PD typically requires highly invasive approaches. Thus, development of non-invasive measures to therapeutically regulate pathogen-driven inflammation and limit oral bone loss are sought to augment current PD clinical treatment modalities. Recent studies have identified that one group of nuclear hormone receptors, peroxisome proliferator-activated receptors (PPARs), as potential molecules of therapeutic value as PPARs have been shown to control expression of genes involved in inflammation. Although some supportive data exists regarding the role played by PPARs in pathogen- induced inflammation, there is a significant gap in our knowledge in the context of PD-associated bacterial infection-elicited inflammation, and oral bone loss. Based on our preliminary data, and the gap in knowledge regarding specific PPAR exploitation as a therapeutic target for controlling Pg infection-elicited inflammation and oral bone loss, we propose that that PPARs control the expression of key inflammatory elements that contribute inflammation and oral bone loss elicited by the defined periodontal pathogen Pg. Our approach, will utilize an in vitro screen employing human tissue resident macrophages and epithelial cells to identify a PPAR agonist or antagonist that most significantly reduces cellular inflammatory response to Pg challenge. This PPAR-targeting molecule will then be tested in an animal model to define its therapeutic value in reducing Pg oral infection- elicited inflammation and oral bone loss.