Obesity and Asthma An Inflammatory Disease of Adipose Tissue Not the Airway
Obesity and Asthma An Inflammatory Disease of Adipose Tissue Not the Airway
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DOI：
10.1164/rccm.201203-0573oc
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发表时间：
2012-10-01
影响因子：
24.7
通讯作者：
Dixon, Anne E.
中科院分区：
文献类型：
--
作者：
Sideleva, Olga;Suratt, Benjamin T.;Dixon, Anne E.
理论基础：肥胖是哮喘的主要危险因素；其原因尚不清楚，尽管人们认为肥胖时脂肪组织中的炎症变化可能导致肥胖个体的呼吸道炎症和气道反应性。目的：确定肥胖中脂肪组织的炎症是否与晚发型哮喘有关，并与呼吸道炎症和反应性标志物增加有关。方法：我们招募了一组患有哮喘的肥胖女性和肥胖对照组女性。我们在减肥手术后对哮喘患者进行了12个月的跟踪调查。我们比较了哮喘患者和对照组的脂肪组织和呼吸道中的标志物，以及哮喘患者随时间的变化。测量和主要结果：当控制体重指数时，哮喘患者内脏脂肪组织的巨噬细胞浸润增加(P<；0.01)，瘦素表达增加(P<；0.01)，脂联素降低(P<；0.001)。在皮下脂肪组织中也观察到类似的趋势。呼吸道上皮细胞表达瘦素和脂联素受体，呼吸道反应性与内脏脂肪瘦素表达显著相关(Rho=-0.8；P<；0.01)。哮喘患者的肺泡灌洗液细胞因子和肺泡巨噬细胞产生的细胞因子在基线时与对照组相似，术后12个月趋于增加。结论：肥胖与血清和脂肪组织中炎症标志物的增加有关，但却降低了哮喘患者的呼吸道炎症；这些模式随着减肥手术的进行而逆转。瘦素和其他脂肪因子可能通过直接作用于呼吸道而不是通过增强呼吸道炎症而成为肥胖症中呼吸道疾病的重要介质。
Rationale: Obesity is a major risk factor for asthma; the reasons for this are poorly understood, although it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in individuals who are obese.Objectives: To determine if inflammation in adipose tissue in obesity is related to late-onset asthma, and associated with increased markers of airway inflammation and reactivity.Methods: We recruited a cohort of obese women with asthma and obese control women. We followed subjects with asthma for 12 months after bariatric surgery. We compared markers in adipose tissue and the airway from subjects with asthma and control subjects, and changes in subjects with asthma over time.Measurements and Main Results: Subjects with asthma had increased macrophage infiltration of visceral adipose tissue (P < 0.01), with increased expression of leptin (P < 0.01) and decreased adiponectin (p < 0.001) when controlled for body mass index. Similar trends were observed in subcutaneous adipose tissue. Airway epithelial cells expressed receptors for leptin and adiponectin, and airway reactivity was significantly related to visceral fat leptin expression (rho = -0.8; P < 0.01). Bronchoalveolar lavage cytokines and cytokine production from alveolar macrophages were similar in subjects with asthma and control subjects at baseline, and tended to increase 12 months after surgery.Conclusions: Obesity is associated with increased markers of inflammation in serum and adipose tissue, and yet decreased airway inflammation in obese people with asthma; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease in obesity through direct effects on the airway rather than by enhancing airway inflammation.