Mouse Allergen and Asthma Intervention Trial

说明(申请人提供)哮喘是最常见的慢性病之一，它对居住在城市地区的弱势群体的影响不成比例。尤其是老鼠过敏原暴露，似乎在城市哮喘流行中起着关键作用，原因有几个：(1)Mus m1是主要的老鼠过敏原，在95%的市中心家庭中发现，并且在市中心家庭中的浓度是郊区家庭的100倍；(2)在城市地区的哮喘儿童中，多达25%-50%的儿童有证据表明对老鼠的IgE敏感，使他们容易出现老鼠过敏原引发的哮喘症状；(3)在对IgE敏感的哮喘儿童中，家鼠变应原暴露与更多的症状天数、更多的抢救药物使用和更多的哮喘相关医疗保健使用有关。虽然这些都是令人信服的观察结果，但证明减少小鼠过敏原暴露可改善小鼠致敏哮喘儿童的哮喘健康状况，对于确定小鼠过敏原暴露的因果作用至关重要。初步证据表明，小鼠变应原靶向环境干预(MA-EI)有效地将尘埃MUM1水平降低75%；提供了最后一段背景数据，支持MA-EI将降低患有哮喘的小鼠致敏个体的哮喘发病率的假设。为了验证这一假设，我们建议在哮喘和老鼠致敏高患病率以及家庭Mus m1水平高的美国东北部两个主要城市中心进行MA-EI的多中心随机临床试验。目的1：确定这种MA-IE的有效性：(A)减少哮喘症状和挽救药物使用，(B)减少与哮喘相关的医疗保健利用，以及(C)改善小鼠致敏哮喘儿童哮喘疾病活动的生理和炎症标记物。目的2：评价小鼠特异性免疫球蛋白Ig G和免疫球蛋白E作为过敏原暴露和哮喘临床状态的生物标志物。临床试验的结果将有助于深入了解家鼠过敏原暴露对城市哮喘人群的影响，并直接为公共卫生战略提供信息，以减轻市中心的哮喘负担。

DESCRIPTION (provided by applicant) Asthma is one of the most common chronic illnesses and it disproportionately affects disadvantaged populations residing in urban areas. Mouse allergen exposure, in particular, appears to play a critical role in the urban asthma epidemic for several reasons: (1) Mus m 1, the major mouse allergen, is found in 95% of inner-city homes, and is found in 100-fold higher concentrations in inner-city homes than in suburban homes; (2) As many as 25-50% of children with asthma living in urban areas have evidence of IgE-sensitization to mouse, making them susceptible to mouse allergen-triggered asthma symptoms; and (3) Home mouse allergen exposure is associated with more symptoms days, more rescue medication use, and more asthma related health care use among IgE-sensitized children with asthma. Although these are compelling observations, demonstrating that a reduction of mouse allergen exposure results in Improved asthma health in mouse-sensitized children with asthma is critical for establishing a causal role for mouse allergen exposure. Preliminary evidence indicating that a mouse allergen-targeted environmental intervention (MA-EI) is efficacious in reducing settled dust Mus m 1 levels by >75% provides the final piece of background data to support the hypothesis that a MA-EI will reduce asthma morbidity in mouse-sensitized individuals with asthma. To test this hypothesis, we propose conducting a multi-center, randomized clinical trial of MA-EI at two major Northeastern US urban centers with high prevalence of asthma and mouse sensitization and high home Mus m 1 levels. Aim 1 is: To determine the efficacy of this MA-IE to: (a) Reduce asthma symptoms and rescue medication use, (b) Reduce asthma-related health care utilization, and (c) Improve physiologic and inflammatory markers of asthma disease activity among mouse-sensitized children with asthma. Aim 2 is: To evaluate mouse-specific IgG and IgE as biomarkers of allergen exposure and asthma clinical status. The findings from the clinical trial will lend critical insight into the impact of home mouse allergen exposure on urban populations with asthma, and directly inform public health strategies to reduce the inner-city asthma burden.