Abstract：
Obesity is a contributing factor to asthma severity; while it has long been understood that obesity is related to greater asthma burden, the mechanisms though which this occurs have not been fully elucidated. One common explanation is that obesity mechanically reduces lung volume through accumulation of adipose tissue external to the thoracic cavity. However, it has been recently demonstrated that there is substantial adipose tissue within the airway wall itself, and that the presence of adipose tissue within the airway wall is related to body mass index. This suggests the possibility of an additional mechanism by which obesity may worsen asthma, namely by altering the behaviour of the airways themselves. To this end, we modify Anafi & Wilson\'s classic model of the bistable terminal airway to incorporate adipose tissue within the airway wall in order to answer the question of how much adipose tissue would be required in order to drive substantive functional changes. This analysis suggests that adipose tissue within the airway wall on the order of 1%-2% of total airway cross-sectional area could be sufficient to drive meaningful changes, and further that these changes may interact with volume effects to magnify the overall burden.
摘要：
肥胖是导致哮喘严重程度的一个因素；虽然人们早就知道肥胖与更大的哮喘负担有关，尽管发生这种情况的机制尚未完全阐明。一种常见的解释是肥胖通过胸腔外部的脂肪组织的积累而机械地减少肺体积。然而,最近已经证明，气道壁本身内有大量的脂肪组织，气道壁内脂肪组织的存在与体重指数有关。这表明肥胖可能导致哮喘恶化的另一种机制的可能性，即通过改变气道本身的行为。为此,我们修改了Anafi&Wilson的双稳态终末气道的经典模型,使其在气道壁内加入脂肪组织,以回答需要多少脂肪组织来驱动实质性功能改变的问题。该分析表明，气道壁内的脂肪组织占总气道横截面积的1%-2%，足以驱动有意义的变化。此外，这些变化可能会与体积效应相互作用，以放大整体负担。
