COMPARATIVE PROTEOMIC INVESTIGATION OF ARDS AND SYSTEMIC INFLAMMATORY INJURY

ARDS 和全身炎症损伤的比较蛋白质组学研究

• 批准号: 7601816
• 负责人: MICHAEL A. MATTHAY
• 金额: $ 0.07万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-09-30 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7601816
• 关键词: Adult Respiratory Distress Syndrome; Alveolar; Animals; Blood Proteins; Blood capillaries; Cells; Clinical; Clinical Research; Computer Retrieval of Information on Scientific Projects Database; Control Animal; Disease; Evaluation; Funding; Grant; Inflammatory; Inflammatory Response; Injury; Institution; Intensive Care; Investigation; Ischemia; Kupffer Cells; Liquid substance; Liver; Lung; Mechanical ventilation; Medicine; Morbidity - disease rate; Patients; Physiological reperfusion; Pneumonia; Proteome; Proteomics; Pulmonary Edema; Pulmonary aspiration of gastric contents; Rattus; Reaction; Reperfusion Injury; Reperfusion Therapy; Research; Research Personnel; Resources; Sampling; Sepsis; Source; Tidal Volume; Trauma; United States National Institutes of Health; Ventilator-induced lung injury; alveolar type II cell; capillary; comparative; improved; mortality

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. The acute respiratory distress syndrome (ARDS) is one of the most important causes for morbidity and mortality in intensive care medicine. It can be the sequel of diseases like sepsis, aspiration of gastric contents, pneumonia or trauma. It is characterized by an inflammatory reaction that leads to a breakdown of the alveolar-capillary barrier, resulting in an influx of fluid and proteins from the blood into the alveolar space. The exact mechanism of the inflammatory reaction is still incompletely understood. Numerous clinical and experimental trials have been made in order to improve the understanding and evaluate possible treatment options. It has been shown in clinical studies that the mode of mechanical ventilation, namely the tidal volume that is used, impacts survival of patients with this disease. The focus of our studies was on three different aspects: - The evaluation of pulmonary edema fluid samples of patients with ARDS compared to control samples - Induction of ventilator induced lung injury in rats and comparison of the proteome of alveolar type II cells from these animals with cells from not ventilated control animals - Induction of liver damage in rats by ischemia-reperfusion and evaluation of the proteome of the pulmonary alveolar type II cells to investigate the influence of a systemic inflammatory response on the proteome of these cells - In an additional project in cooperation with the UCSF liver center, proteomic changes in inflammatory cells were investigated. This was done using isolated Kupffer cells from rats with ischemia-reperfusion injury.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 急性呼吸窘迫综合征（ARDS）是重症监护医学中发病和死亡率的最重要原因之一。它可以是败血症，胃含量，肺炎或创伤等疾病的续集。它的特征是炎症反应，导致肺泡毛细血管屏障的分解，从而导致流体和蛋白质从血液流入到肺泡空间中。炎症反应的确切机制仍未完全理解。为了提高理解并评估可能的治疗选择，已经进行了许多临床和实验试验。在临床研究中已经表明，机械通气的模式，即所使用的潮汐体积会影响该疾病患者的存活。 我们研究的重点是三个不同方面： - 与对照样品相比，ARDS患者的肺水肿流体样品的评估 - 诱导呼吸机诱导的大鼠肺损伤，并比较这些动物的肺泡II型细胞的蛋白质组与非通风对照动物的细胞的蛋白质组 - 通过缺血 - 再灌注和评估肺肺泡II型细胞的蛋白质组来诱导大鼠肝损伤，以研究全身炎症反应对这些细胞蛋白质组的影响 - 在与UCSF肝脏中心合作的另一个项目中，研究了炎症细胞的蛋白质组学变化。这是使用来自缺血 - 再灌注损伤的大鼠分离的库普弗细胞完成的。