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

西方饮食的后果之一是呼吸道高反应性(AH)，表现为肥胖相关的哮喘。除了与急性肺损伤有关的巨噬细胞的改变外，我们还观察到肺内脂质堆积和基质细胞成分的改变。在此，我们认为肺巨噬细胞和间质细胞由脂质环境编程在AH的发生发展中起协同作用。该项目将定义这些分子途径，并剖析这些细胞的贡献以及它们在AH过程中的串扰。这些数据将确定驱动这种疾病的关键机制，从而使潜在的新的有针对性的治疗急性肝炎成为可能。

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.