EFFECT OF SIMVASTATIN ON CYSTIC FIBROSIS AIRWAY INFLAMMATION

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 患有囊性纤维化（CF）的个体在气道中具有持续感染，身体试图通过招募免疫细胞（中性粒细胞）到肺部来对抗感染。免疫系统和中性粒细胞无法完全杀死细菌，对感染的反应导致气道炎症（肿胀）和肺损伤。一氧化氮（NO）在肺中具有抗菌和抗炎特性。CF患者NO生成减少，可能与持续感染和炎症有关。增加CF患者气道中NO的产生可能有助于减少这种炎症和感染。本研究将检验以下假设：给予辛伐他汀（舒降之）将增加囊性纤维化受试者呼出的一氧化氮（eNO）并减少气道炎症标志物。这是一项多中心、前瞻性研究，旨在检查10岁及以上囊性纤维化（CF）患者口服辛伐他汀（Zocor <$）治疗28天对呼出气一氧化氮和鼻上皮样本及诱导痰样本中气道炎症指标的影响。 本研究还将探索鼻上皮细胞作为下气道炎症的替代标记物的用途。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Individuals with cystic fibrosis (CF) have persistent infection in the airways, which the body attempts to fight by recruiting immune cells (neutrophils) to the lung. The immune system and neutrophils are unable to completely kill the bacteria, and the response to the infection leads to inflammation (swelling) of the airways and lung damage. Nitric oxide (NO) has anti-bacterial and anti-inflammatory properties in the lung. NO production is decreased in CF patients, and may contribute to the persistent infection and inflammation. Increasing the production of NO in the airways of CF patients may help decrease this inflammation and infection. This study will test the hypothesis that the administration simvastatin (Zocor¿) will increase exhaled nitric oxide (eNO) and decrease markers of airway inflammation in subjects with cystic fibrosis. This is a multi-center, prospective study examining the effects of 28 days of oral simvastatin (Zocor¿) treatment on exhaled nitric oxide and measures of airway inflammation in nasal epithelial samples and induced sputum samples in patients with cystic fibrosis (CF) ages 10 and older. This study will also explore the use of nasal epithelial cells as surrogate markers for lower airway inflammation.