Immune and stromal dysregulation by excess dietary lipids leading to airway hyperresponsiveness (P12)

西方饮食的后果之一是气道高反应性（AH），表现为肥胖相关的哮喘。除了与AH有关的巨噬细胞的改变外，我们还观察到肺中脂质积累和基质细胞组成的改变。在这里，我们提出肺巨噬细胞和脂质环境编程的基质细胞在AH的发展中协同作用。该项目将定义这些分子途径，并剖析这些细胞及其在AH期间的串扰的贡献。这些数据将确定驱动该疾病的关键机制，从而使潜在的新的AH靶向治疗成为可能。

One of the consequences of Western diet is airway hyperreactivity (AH), which manifests itself as obesity-associated asthma. Besides the alteration of macrophages, that have been implicated in AH, we observed lipid accumulation and altered stromal cell composition in the lung. Here, we propose that pulmonary macrophages and stromal cells programmed by the lipid milieu synergize in the development of AH. The project will define these molecular pathways and dissect the contribution of these cells and their crosstalk during AH. The data will identify key mechanisms that drive the disease and will thereby enable potential new targeted therapies for AH.