Traffic-related air pollutants and respiratory tract microbiome in children

儿童交通相关空气污染物和呼吸道微生物组

• 批准号: 9144397
• 负责人: ATIN ADHIKARI
• 金额: $ 24.09万
• 依托单位: UNIVERSITY OF CINCINNATI
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-09-30 至 2018-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9144397
• 关键词: Adherence; Adolescent; Adult; Affect; Age; Air Pollutants; Air Pollution; Allergens; Allergic; Asthma; B-Lymphocytes; Bacteria; Bacterial Infections; Bacterial Pneumonia; Birth; Carbon nanoparticle; Categories; Cells; Characteristics; Child; Childhood; Clinical; Cohort Studies; Communities; Computer software; DNA; DNA Sequence Analysis; Data; Databases; Dendritic Cells; Development; Enrollment; Environment; Environmental Exposure; Epidemiologic Studies; Epithelial; Epithelial Cells; Etiology; Exposure to; Funding; General Population; Growth; Haemophilus influenzae; Health; High-Throughput Nucleotide Sequencing; Human; Human Microbiome; Hypersensitivity; Immune Tolerance; Immune response; Immune system; Incidence; Indigenous; Intervention; Lead; Life; Lower respiratory tract structure; Lung; Lung diseases; Metagenomics; Modeling; Molds; Moraxella (Branhamella) catarrhalis; Mus; National Institute of Environmental Health Sciences; Nature; Neonatal; Oxidative Stress; Play; Predisposition; Publishing; Reading; Recruitment Activity; Recurrence; Regulatory T-Lymphocyte; Reporting; Research; Research Personnel; Respiratory System; Respiratory tract structure; Ribosomal RNA; Risk; Role; Sampling; Shapes; Sputum; Streptococcus pneumoniae; Structure of parenchyma of lung; Technology; Time; Upper Respiratory Infections; Wheezing; airborne allergen; allergic response; arm; asthmatic; asthmatic airway; base; cell injury; cohort; cytokine; deep sequencing; early adolescence; fungus; gut microbiota; indexing; infancy; land use; microbial; microbiome; microbiota; microorganism; multidisciplinary; particle; respiratory; respiratory health; response; traffic-related air pollution; trafficking

 DESCRIPTION (provided by applicant): The interplay between environmental exposures, respiratory tract microbiome, and immune responses related to asthma and other respiratory diseases is not well understood. High levels of traffic-related air pollutants (TRAP) have been associated with children's asthma. TRAP can increase adherence of microorganisms to the epithelial cells of the respiratory tract and damage the epithelial layers resulting in increased susceptibility to microbial growth. Many studies suggest a role for altered human microbiota in the etiology of asthma. Furthermore, circumstantial evidence indicates that bacterial infections in the respiratory tract may play a role in asthma development. The airway microbiota may interact with the innate and adaptive arms of the children's developing mucosal immune system in the respiratory tract, which can be critically important in maintaining tolerance against allergc immune responses. Our recent data show that increased exposure to traffic-related particles at birth is associated with longitudinal childhood wheezing. We hypothesize that exposure to TRAP early in life significantly alters the diversity of microorganisms in the respiratory tract in chilren and this effect persists to early adolescence. In Specific Aim 1, we will characterize the respiratory tract microbiome of adolescent children exposed to high and low levels of traffic related air pollution during childhood. Children from the existing cohort of the NIEHS-funded Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) will be recruited for this purpose. This cohort is well characterized regarding childhood exposure to TRAP and indoor aeroallergens as well respiratory health of children from birth to age 12. TRAP exposure at ages 12-15 will be estimated by a land use regression (LUR) model of exposure to truck and bus traffic. Bacterial composition, operational taxonomic units (OTUs), and diversity indices in the respiratory tract of children will be characterized by collecting induced sputum samples, extracting DNA, amplifying bacteria-specific PCR products (using 16S rRNA primers), analyzing DNA sequences by deep sequencing, clustering and assignment of Illumina MiSeq reads into Operational Taxonomic Units (OTUs), analysis of OTUs, and determination of bacterial diversity by RDP database and pipeline, as well as MG-RAST and Qiime software packages. In Specific Aim 2, we will assess associations between bacterial OTUs, diversity indices, and TRAP. To our knowledge, there are no previous reports on the effects of air pollutants on the human respiratory tract microbiome, particularly among children. This information is critically important to understand the interaction between air pollution, human microbiome, and respiratory health among children.

 描述（由申请人提供）：环境暴露、呼吸道微生物群以及与哮喘和其他呼吸道疾病相关的免疫反应之间的相互作用尚不清楚。高水平的交通相关空气污染物（TRAP）与儿童哮喘有关。 TRAP 可以增加微生物对呼吸道上皮细胞的粘附，并损伤上皮层，导致微生物生长的敏感性增加。许多研究表明，它对人类有一定作用。此外，间接证据表明，呼吸道细菌感染可能在哮喘发展中发挥作用，气道微生物群可能与儿童呼吸道中正在发育的粘膜免疫系统的先天性和适应性相互作用。这对于维持对过敏免疫反应的耐受性至关重要。我们最近的数据表明，出生时接触交通相关颗粒的增加与童年时期纵向喘息的发生密切相关。改变儿童呼吸道微生物的多样性，并且这种影响持续到青春期早期。在具体目标 1 中，我们将描述童年时期暴露于高水平和低水平交通相关空气污染的青少年儿童的呼吸道微生物组。为此目的，将招募 NIEHS 资助的辛辛那提儿童过敏和空气污染研究 (CCAAPS) 的现有队列。该队列在儿童接触 TRAP 和室内空气过敏原方面具有良好的特征。以及从出生到 12 岁儿童的呼吸系统健康状况。12-15 岁的 TRAP 暴露将通过卡车和公共汽车交通暴露的土地利用回归 (LUR) 模型、操作分类单位 (OTU) 和细菌成分来估计。通过采集诱导痰样本、提取DNA、扩增细菌特异性PCR产物（使用16S rRNA引物）、深度测序分析DNA序列、聚类分析，对儿童呼吸道多样性指数进行表征Illumina MiSeq 读取操作分类单元 (OTU) 的分配、OTU 分析以及通过 RDP 数据库和管道以及 MG-RAST 和 Qiime 软件包确定细菌多样性。在特定目标 2 中，我们将评估之间的关联。据我们所知，之前没有关于空气污染物对人类呼吸道微生物群影响的报道，特别是对儿童而言。 了解空气污染、人类微生物组和儿童呼吸系统健康之间的相互作用。