WEIGHT LOSS & ASTHMA

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 流行病学和基础科学研究有非常有力的证据表明，肥胖可能会增加患哮喘的风险。 鉴于目前肥胖和哮喘的并行流行，这对美国人口的健康具有非常重要的意义。 了解肥胖引起的生理和炎症变化将对我们理解肥胖和哮喘之间的关系做出重要贡献。同样重要的是要理解为什么有些肥胖的人会患上哮喘，而另一些人则不会。 我们假设，与没有哮喘的肥胖者相比，患有哮喘的肥胖者改变了脂肪组织相关的炎症。 我们还假设体重减轻将改善哮喘的生理和炎症指标 我们已经组建了一个多学科团队，包括外科医生，内分泌学家和肺病学家，以研究因极度肥胖而接受胃旁路手术的患者。 我们正在研究手术前和手术后12个月的肥胖哮喘患者：我们正在研究（i）手术前后采用复杂的生理技术的肺功能（ii）通过对手术时收集的内脏和皮下脂肪进行体外研究的脂肪相关炎症（iii）脂肪组织产生的循环促炎因子和（iv）通过支气管镜检查观察肺部炎症，并通过支气管肺泡灌洗分离细胞进行体外研究。 作为一个对照组，我们也在研究没有哮喘的肥胖患者，以确定是否有脂肪组织相关因素的差异，可以解释为什么他们没有哮喘。

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. There is very strong evidence from epidemiological and basic science studies to suggest that obesity may increase the risk of asthma. This has very important implications for the health of the US population given the current parallel epidemics of obesity and asthma. Understanding the physiological and inflammatory changes induced by obesity would make an important contribution to our understanding of the relationship between obesity and asthma. It is also important to understand why some obese people develop asthma, but others do not. We hypothesize that obese people with asthma have altered adipose tissue related inflammation compared to obese people without asthma. We also hypothesize that weight loss will improve physiological and inflammatory measures of asthma We have assembled a multi-disciplinary team, including surgeons, endocrinologists and pulmonologists to study patients undergoing gastric bypass surgery for extreme obesity. We are studying obese patients with asthma before surgery and in the 12 months after surgery: we are studying (i) their lung function with sophisticated physiological techniques before and after surgery (ii) adipose-related inflammation by in vitro studies on visceral and subcutaneous fat collected at the time of surgery (iii) circulating pro-inflammatory factors produced by adipose tissue and (iv) inflammation in the lung by bronchoscopy with isolation of cells by bronchoalveolar lavage for in vitro studies. As a comparison group we are also studying obese patients without asthma to determine if there are differences in adipose tissue-related factors that could explain why they do not have asthma.