EFFECT OF LINOLEIC ACID ON INFLAMMATORY MARKERS IN CYSTIC FIBROSIS

亚油酸对囊性纤维化炎症标志物的影响

• 批准号: 7718943
• 负责人: Steven David Freedman
• 金额: $ 0.01万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-04-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7718943
• 关键词: Adult; Affect; Arachidonic Acids; Blood; Characteristics; Computer Retrieval of Information on Scientific Projects Database; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Defect; Diet; Disease; Funding; Gene Mutation; Grant; Heterozygote; Immune response; Inflammatory; Inflammatory Response; Institution; Linoleic Acids; Measurement; Mediator of activation protein; Mutation; Research; Research Personnel; Resources; Risk; Source; Sputum; Testing; United States National Institutes of Health; base; fatty acid metabolism; novel therapeutics; therapeutic target

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 underlying hypothesis for this study is that dysregulation of fatty acid metabolism which is magnified by increased linoleic acid levels, leads to the excessive inflammatory response characteristic of Cystic Fibrosis (CF) and represents a novel therapeutic target. In addition, healthy obligate heterozygotes (carriers of a CF gene mutation) display a similar defect in fatty acid metabolism and innate immune response. In addition, heterozygotes are at risk for adult onset inflammatory disorders. This hypothesis will be tested by determining if increased linoleic acid in the diet of subjects with one disease associated severe CFTR mutation (healthy obligate heterozygotes) or two severe CFTR mutations (classic CF) increases Arachidonic Acid (AA) levels and downstream inflammatory mediators based on measurements in blood and in CF subjects, also in induced sputum. These results will be compared to healthy subjects with no CFTR mutations where AA levels should be tightly controlled and not significantly affected by linoleic acid levels in the diet.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 这项研究的基本假设是，脂肪酸代谢失调会因亚油酸水平增加而加剧，导致囊性纤维化 (CF) 的过度炎症反应特征，并代表了一个新的治疗靶点。此外，健康的专性杂合子（CF 基因突变的携带者）在脂肪酸代谢和先天免疫反应方面也表现出类似的缺陷。此外，杂合子存在成人发病炎症性疾病的风险。该假设将通过确定患有一种与严重 CFTR 突变（健康专性杂合子）或两种严重 CFTR 突变（经典 CF）相关疾病的受试者的饮食中增加的亚油酸是否会增加花生四烯酸（AA）水平和下游炎症介质来进行检验。血液和 CF 受试者以及诱导痰中的测量。这些结果将与没有 CFTR 突变的健康受试者进行比较，其中 AA 水平应受到严格控制，并且不会受到饮食中亚油酸水平的显着影响。