Analysis of lipids, inflammation, and pulmonary function

慢性阻塞性肺疾病（COPD）似乎是由远端细支气管的慢性炎症引起的，尽管我们对慢性阻塞性肺疾病作为一种全身性炎症的认识仍然很初级。血清脂质似乎与多种炎症有关，仍处于初级阶段。血脂似乎与多种炎症过程有关，包括动脉粥样硬化，炎症可能是LDL-胆固醇促进动脉粥样硬化的致病机制。最近的横断面人口数据表明，血脂和肺功能之间存在联系。然而，没有关于血脂与纵向肺功能下降关系的数据报道。此外，关于血脂与血清炎症标志物之间的关系或血脂测量与炎症标志物之间作为肺功能预测因子的潜在相互作用的数据报道很少。我们建议通过使用Framingham心脏研究（FHS）数据来检查血脂和炎症标志物与肺功能损害的关系，以实现以下具体目的：目的1检查血清总胆固醇和脂质亚组分与肺功能的横断面和纵向关系。在调整潜在混杂因素后，我们将采用多变量模型来确定总胆固醇和脂质亚组分是否与肺功能水平和下降速率独立相关。目的#2检查血清炎症标志物（c反应蛋白（CRP）、纤维蛋白原和血清淀粉样蛋白A）与肺功能的横断面和纵向关系。在调整潜在混杂因素后，我们将采用多变量模型来确定这些全身性炎症标志物是否与肺功能水平和下降速度独立相关。目的#3评估血脂亚组分和血清炎症标志物之间的潜在相互作用，作为肺功能下降水平和速度的预测因子。我们将采用多变量模型来确定血清炎症标志物是否与血脂水平独立相关，并检查血脂亚组分和血清炎症标志物在预测肺功能下降水平和速度方面可能存在的相互作用。

Chronic obstructive pulmonary disease (COPD) appears to result from chronic inflammation of the distal bronchioles, although our understanding of COPD as a disease of systemic inflammation remains rudimentary. Serum lipids appears to be related to a variety of inflammatory remains rudimentary. Serum lipids appear to be related to a variety of inflammatory processes, including atherosclerosis, and inflammatory may be the pathogenic mechanisms by which LDL- cholesterol promotes atherosclerosis. Recent cross-sectional population data have suggested a link between serum-lipids and pulmonary function . No data have been reported, however, on the relation of serum lipids to longitudinal pulmonary function decline. Furthermore, few data have been reported on the relation of serum lipids to serum inflammatory markers or on potential interactions between serum lipid measurements and markers of inflammation as predictors of pulmonary function. We propose to examine the relation of serum lipids and inflammatory markers to pulmonary function impairment by using Framingham Heart Study (FHS) data to pursue the following specific aims: Aim 1 Examine the cross-sectional and longitudinal relation of serum total cholesterol and lipid sub-fractions to pulmonary function. We will employ multi-variate models to determine if total cholesterol and lipid sub-fractions are independently associated with pulmonary function level and rate of decline, after adjustment for potential confounders. Aim #2 Examine the cross-sectional and longitudinal relation of serum markers of inflammation (c-reactive protein (CRP), fibrinogen, and serum amyloid A to pulmonary function. We will employ multi-variate models to determine if these markers of systemic inflammation are independently associated with pulmonary function level and rate of decline, after adjustment for potential confounders. Aim #3 Assess the potential interaction between lipid sub-fractions and serum markers of inflammation as predictors of the level and rate of decline of pulmonary of pulmonary function. We will employ multi- variate models to determine if serum markers of inflammation are independently related to serum lipid levels, and to examine possible interactions between lipid sub-fractions and serum markers of inflammation in predicting level and rate of decline of pulmonary function.