Children's Respiratory and Environmental Workgroup (CREW)

儿童呼吸和环境工作组 (CREW)

• 批准号: 10011947
• 负责人: James E. Gern
• 金额: $ 1141.82万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-09-21 至 2023-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10011947
• 关键词: Address; Affect; Age; Allergens; Asthma; Bacteria; Bayesian Network; Biogenesis; Biological Markers; Birth; Cataloging; Catalogs; Child; Childhood Asthma; Chronic; Clinical; Cohort Studies; Data; Data Collection; Data Discovery; Data Element; Data Set; Databases; Development; Disease remission; Dose; Enrollment; Environment; Environmental Exposure; Environmental Risk Factor; Epigenetic Process; Ethnic Origin; Etiology; Event; Family; FarGo; Foundations; Future; Genetic; Geographic Information Systems; Goals; Health; Immunologics; Incidence; Individual; Infection; Integration Host Factors; Laboratories; Life; Life Style; Longterm Follow-up; Measurement; Measures; Medical; Meteorology; Methods; Molecular; Neighborhoods; Outcome; Participant; Pathogenesis; Pattern; Phenotype; Physical environment; Plant Roots; Population Characteristics; Pregnant Women; Prevalence; Procedures; Psychosocial Stress; Race; Recommendation; Recording of previous events; Research; Research Personnel; Resources; Risk; Risk Factors; Sample Size; Sampling; Socioeconomic Status; Standardization; Surveys; Syndrome; System; Systems Analysis; Time; Viral Respiratory Tract Infection; Virus; Work; advanced analytics; asthma exacerbation; asthma prevention; base; cohort; data harmonization; digital; disorder prevention; early childhood; early life exposure; individualized prevention; information model; innovation; microbiome; molecular marker; novel; pollutant; prenatal; prevent; prospective; psychosocial; pulmonary function; resilience; respiratory; respiratory health; sample collection; sex; socioeconomic disadvantage; standardize measure; young adult

PROJECT SUMMARY/ABSTRACT Individual birth cohort studies have identified risk factors for developing childhood asthma, including environmental exposures in early life such as allergens, pollutants, patterns of infection and colonization with viruses and bacteria, and psychosocial stress. Despite such advances, further progress in understanding the root causes of asthma have been hampered by at least two factors. First, procedures and scientific methods are not standardized across cohorts, making it difficult to compare and validate findings. Second, asthma definitions across cohorts vary considerably. In fact, asthma is a syndrome; there are different subtypes of asthma with distinct clinical features (“asthma phenotypes”) and likely different etiologies (“asthma endotypes”). We hypothesize that host factors (genetics, epigenetics) interact with environmental exposures during the prenatal period and early childhood to cause specific endotypes of childhood asthma. We further propose that identification of endotypes and associated molecular biomarkers in early life can provide a new paradigm for asthma prevention. Unfortunately, single cohorts have limited ability to identify asthma endotypes due to small sample size and unique population characteristics. To overcome shortcomings of individual cohorts, investigators leading 12 asthma birth cohorts across the U.S. now propose the establishment of the Children's Respiratory Research and Environment Workgroup (“CREW”) consortium. This consortium proposes to identify asthma endotypes and overcome shortcomings of individual cohorts by: 1) providing a large (nearly 9000 births and long-term follow-up of 6000-7000 children and young adults) and diverse national data set, 2) harmonizing data related to asthma clinical indicators and early life environmental exposures, 3) developing standardized measures for prospective data collection across CREW cohorts and other ECHO studies, and 4) conducting targeted enrollment of additional subjects into existing cohorts. This approach will enable collection of samples that are optimized for a systems approach to understanding how environmental and host factors in early life promote the development of specific asthma endotypes. Collectively, the results of this comprehensive research to identify the root causes of asthma vs. resilience and health will go far beyond what can be accomplished by individual cohorts, and thus provide a foundation for future efforts aimed at personalized prevention of chronic childhood asthma.

项目概要/摘要 个别出生队列研究已确定了发生儿童哮喘的危险因素，包括 生命早期的环境暴露，例如过敏原、污染物、感染模式和定植 尽管取得了这些进展，但在了解病毒和细菌以及心理社会压力方面仍取得了进一步进展。 哮喘的根源至少受到两个因素的阻碍：第一，程序和科学方法。 不同队列之间的数据没有标准化，因此很难比较和验证研究结果。 其次，哮喘。 事实上，哮喘是一种综合征，有不同的亚型。 具有不同临床特征（“哮喘表型”）和可能不同病因（“哮喘 我们努力探究宿主因素（遗传学、表观遗传学）与环境的相互作用。 产前和儿童早期的暴露导致儿童特定的内型 我们进一步建议在生命早期鉴定内型和相关分子生物标志物。 可以为哮喘预防提供新的范例，不幸的是，单一队列的识别能力有限。 克服了哮喘内型由于样本量小和独特的人群特征的缺点。 在美国各地领导 12 个哮喘出生队列的研究人员现在提出 儿童呼吸研究和环境工作组（“CREW”）联盟的成立。 联盟建议通过以下方式识别哮喘内型并克服个体群体的缺点：1) 提供大量（近 9000 名新生儿和 6000-7000 名儿童和青少年的长期随访）和 不同的国家数据集，2) 协调与哮喘临床指标和早期生活环境相关的数据 3) 制定跨 CREW 群体的前瞻性数据收集的标准化措施，以及 其他 ECHO 研究，以及 4) 有针对性地将其他受试者纳入现有队列。 方法将能够收集针对系统方法进行优化的样本，以了解如何 生命早期的环境和宿主因素促进特定哮喘内型的发展。 总的来说，这项综合研究的结果旨在确定哮喘的根本原因与恢复能力和 健康将远远超出单个群体所能实现的目标，从而为 未来的目标是个性化预防慢性儿童哮喘。