Center for Childhood Asthma in the Urban Environment

城市环境儿童哮喘中心(CCAUE)的长期目标是了解室内和室外空气颗粒物和过敏原暴露如何导致巴尔的摩市中心哮喘儿童的呼吸道炎症和呼吸道发病率，并确定减少与这些暴露相关的发病率的新机会和新策略。指导该中心拟议研究的首要假设是，室内空气污染(颗粒物和过敏原)会导致氧化应激增加，从而导致儿童呼吸道炎症和哮喘发病率增加。研究人员已经组建了一个多学科的综合研究团队，研究氧化应激和呼吸道炎症在哮喘发病中的作用，以开发新的效应生物标志物，提供对易感基因的洞察，提供更好的临床管理，并确定干预机会(环境和药物)。 该计划概述了一个多学科计划，旨在解决这一假设和长期目标。该中心的应用包括以下两个面向临床和面向机械的研究项目： 面向临床的研究项目： 项目1--家庭室内PM与儿童哮喘发病率； 项目2-PM鼻部挑战期间的氧化应激/炎症；以及 机械导向的研究项目： 项目3-Nrf2依赖于哮喘氧化应激的调节； 项目4-PM诱导树突状细胞激活的机制。

The long-term goal of the Center for Childhood Asthma in the Urban Environment (CCAUE) is to understand how exposures to indoor and outdoor airborne particulate matter and allergens may result in airway inflammation and respiratory morbidity in children with asthma living in the inner city of Baltimore and to identify novel opportunities and strategies to reduce morbidity associated with these exposures. The overarching hypothesis guiding the Center's proposed research is that indoor air pollution (particulate matter and allergens) produces increased oxidative stress which leads to increased airway inflammation and asthma morbidity in children. The investigators have assembled a multidisciplinary and integrated team of researchers to investigate the role oxidative stress, and airway inflammation in asthma morbidity in order to develop new biomarkers of effect, provide insight into susceptible genotypes, offer better clinical management, and to identify opportunities for intervention (environmental and pharmacologic). This program outlines a multidisciplinary program directed to address this hypothesis and long-term goal. This Center application includes the following two clinically-oriented and mechanistically-oriented research projects: Clinically-Oriented Research Projects: Project 1 - Domestic Indoor PM and Childhood Asthma Morbidity; Project 2 - Oxidative Stress/Inflammation during PM Nasal Challenge; and Mechanistically-Oriented Research Projects: Project 3 - Nrf2 Dependent Regulation of Oxidative Stress in Asthma; Project 4 - Mechanisms of PM-Induced Dendritic Cell Activation.