Leukotriene Receptor Gene Variation and Atopic Asthma

白三烯受体基因变异与特应性哮喘

• 批准号: 7673033
• 负责人: Kenneth James Wysocki
• 金额: $ 3.51万
• 依托单位: UNIVERSITY OF ARIZONA
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-04-14 至 2011-05-13
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7673033
• 关键词: Address; Affect; Alleles; Asthma; Biological Markers; Candidate Disease Gene; Caucasians; Caucasoid Race; Chemicals; Child; Clinical; Complex; DNA; Data Collection; Detection; Diagnostic; Discrimination; Disease; Economics; Edema; Education; Enrollment; Eosinophilia; Epidemiologic Studies; Epidemiology; Extrinsic asthma; Female; Fostering; Functional disorder; Gender; Genes; Genetic; Genetic Polymorphism; Genetic Predisposition to Disease; Genetic Research; Genetic Variation; Genomics; Goals; Health; Healthy People 2010; Hypersensitivity skin testing; IgE; Inflammation; Inflammatory; Knowledge; Laboratories; Lead; Leukotriene Receptor; Leukotrienes; Life; Link; Longitudinal Studies; Lung; Lung diseases; Modality; Mucous body substance; Obstructive Lung Diseases; Participant; Pathology; Pathway interactions; Patients; Persons; Pharmaceutical Preparations; Pharmacogenetics; Phenotype; Play; Population; Prevention; Prevention strategy; Principal Investigator; Process; Public Health; Quality of life; Questionnaires; Receptor Gene; Research; Risk; Role; Severities; Sex Characteristics; Skin; Surveys; Test Result; Testing; Traineeship; Translating; United States; United States Dept. of Health and Human Services; United States National Institutes of Health; Variant; Work; atopy; bench to bedside; burden of illness; cysteinyl leukotriene receptor; cysteinyl leukotriene receptor 2; disability; eosinophil; health disparity; high risk; improved; inflammatory marker; innovation; male; novel strategies; programs; research study; respiratory; social; tool; trait

DESCRIPTION (provided by applicant): Atopic asthma is a significant economic and public health problem in the world. The pathway of inflammation leading to atopic asthma is a complex process that includes leukotrienes, leukotriene receptors, eosinophils, and Immunoglobulin E (IgE). Evidence also indicates that over 50% of asthma cases are attributed to atopy and that this percentage is higher in males than females. The rate of asthma is increasing in children. Current treatment modalities are unable to adequately control atopic asthma in all patients. Evidence suggests that genetic variation in leukotriene receptors (CYSTLR1 and CYSTLR2) play a role in the expression of inflammation in atopic disease, airway dysfunction and remodeling in asthma, but most of these findings come from studies of homogenous populations outside the United States. To address this gap in knowledge, this genetic epidemiological research study program will explore whether CYSLTR1 and CYSLTR2 gene variations are associated with inflammatory markers of atopy, with atopic asthma, and with gender utilizing a candidate gene association approach of participants already enrolled in the longitudinal Tucson Epidemiological Study of Airway Obstructive Disease (TESAOD) program. TESAOD is comprised of 13 similar surveys and questionnaires including demographic, disease status, medication use, laboratory test results, pulmonary test results, and other biomarkers. The proposed study will include both secondary analysis of information from TESAOD as well as primary data collection of genetic variations through Taqman allele discrimination from extracted DNA from these participants. This traineeship and research is an opportunity to work with the principal investigator in TESAOD and a unique opportunity to research genetic variations in atopic asthma of up to 1,000 U.S. Caucasian participants enrolled in TESAOD. Applicant, sponsor, and co-sponsor are an excellent match for this study of atopic asthma, inflammation, and genetic variations. This research is in alignment with the National Institute of Health goal of fostering fundamental creative discoveries that extend healthy life and reduce the burdens of illness and disability. The goal of this research study and applicant's long term goal are also aligned with the U.S. Department of Health and Human Services, Healthy People 2010 goal for respiratory disease to promote respiratory health through better prevention, detection, treatment, and education efforts. Understanding the pathology and genetic etiology of atopic asthma through this research will help translate genomic research from bench to bedside and contribute to innovative tailored preventive strategies, diagnostic tools, and therapies for those suffering from atopic asthma.

描述（由申请人提供）：特征性哮喘是世界上重大的经济和公共卫生问题。导致特应性哮喘的炎症途径是一个复杂的过程，其中包括白细胞，白细胞受体，嗜酸性粒细胞和免疫球蛋白E（IgE）。证据还表明，超过50％的哮喘病例归因于特应性，而男性的百分比高于女性。儿童哮喘的发生率正在增加。当前的治疗方式无法充分控制所有患者的特应性哮喘。有证据表明，白三烯受体（CYSTLR1和CYSTLR2）的遗传变异在哮喘中的特应性疾病，气道功能障碍和重塑中起作用，但大多数发现来自美国以外同质种群的研究。为了解决知识的这一差距，该遗传流行病学研究计划将探讨Cysltr1和Cysltr2基因变异是否与特应性哮喘的炎症标记有关，并利用性别的性别基因与参与者的候选基因关联方法已经参与了长期TUCSON TUCSON TRESSEMIGY STRAKINE的参与者的研究。 Tesaod由13个类似的调查和问卷组成，包括人口统计学，疾病状态，药物使用，实验室测试结果，肺部测试结果和其他生物标志物。拟议的研究将包括对TESAOD信息的次级分析，以及通过从这些参与者中提取的DNA歧视的遗传变异的主要数据收集。这项培训和研究是与Tesaod的主要研究人员合作的机会，也是一个独特的机会，可以在特索德（Tesaod）入学的高达1,000名美国高加索人参与者中研究遗传变异。申请人，赞助商和共同赞助商是该研究特应性哮喘，炎症和遗传变异的绝佳匹配。这项研究与国家健康研究所的目标保持一致，该研究所促进了延长健康生活并减轻疾病和残疾负担的基本创造性发现。这项研究研究和申请人的长期目标的目标也与美国卫生和公共服务部，健康人2010年的呼吸道疾病目标保持一致，以通过更好的预防，检测，治疗和教育工作来促进呼吸健康。 通过这项研究了解特应性哮喘的病理和遗传病因将有助于将基因组研究从长凳转变为床边，并为患有特应特应性哮喘患者的创新量身定制的预防策略，诊断工具和疗法做出贡献。