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: 8968715
• 负责人: ATIN ADHIKARI
• 金额: $ 21.79万
• 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 2017-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8968715
• 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; 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; microorganism; multidisciplinary; particle; public health relevance; 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（由适用提供）：对环境暴露，呼吸道微生物组和与哮喘和其他呼吸系统疾病有关的免疫调查之间的相互作用尚不清楚。与交通相关的空气污染物（TRAP）高水平与儿童哮喘有关。陷阱可以增加微生物对呼吸道上皮细胞的依从性，并损害上皮层，从而增加对微生物生长的敏感性。许多研究表明，改变人类微生物群在哮喘病因中的作用。此外，间接证据表明，呼吸道中的细菌感染可能在哮喘发育中起作用。气道微生物群可能会与呼吸道中儿童发育中的粘膜免疫系统的先天和适应性臂相互作用，这对于维持对过敏性免疫反应的耐受性至关重要。我们最近的数据表明，出生时与交通相关的颗粒的暴露增加与纵向儿童时期有关。我们假设生命早期接触陷阱的暴露会显着改变Chilren呼吸道中微生物的多样性，并且这种影响持续到早期青少年。在特定的目标1中，我们将表征青少年儿童的呼吸道微生物组，暴露于儿童时期的交通流量高和低水平的空气污染。为此，将招募来自NIEHS资助的辛辛那提儿童过敏和空气污染研究（CCAAP）的现有队列的儿童。该队列在儿童期暴露于陷阱和室内空气过敏剂以及从出生到12岁的儿童的呼吸健康状况方面具有很好的特征。年龄在12-15岁之间的陷阱暴露将通过土地使用回归（LUR）的卡车和公共汽车交通的模型来估计。细菌组成，操作分类学单位（OTU）和儿童呼吸道中的多样性指标将以收集诱导的痰液样本，提取DNA，提取DNA，提取细菌特异性PCR产物（使用16S rRNA Primers）（使用16S rRNA Primers），通过深度序列进行分析，群集和分配的DNA序列，并将其分配为单位，并分配了序列的DNA序列。 （OTU），OTU分析以及通过RDP数据库和管道对细菌多样性的测定，以及MG-RAST和QIIME软件包。在特定的目标2中，我们将评估OTUS细菌，多样性指数和陷阱之间的关联。据我们所知，以前没有关于空气污染物对人呼吸道微生物组的影响的报道，尤其是在儿童中。这些信息至关重要 了解儿童空气污染，人类微生物组和呼吸健康之间的相互作用。