Low-grade adipose tissue inflammation in patients with mild-to-moderate chronic obstructive pulmonary disease
Low-grade adipose tissue inflammation in patients with mild-to-moderate chronic obstructive pulmonary disease
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DOI：
10.3945/ajcn.111.023911
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发表时间：
2011-12-01
影响因子：
7.1
通讯作者：
Schols, Annemie M. W. J.
中科院分区：
文献类型：
--
作者：
van den Borst, Bram;Gosker, Harry R.;Schols, Annemie M. W. J.
背景：低级别全身性炎症在慢性阻塞性肺疾病（COPD）中很常见，但其来源尚不清楚。脂肪组织是炎症介质的有力生产者，可能通过缺氧导致慢性阻塞性肺病的全身性炎症。目的：探讨慢性阻塞性肺病（COPD）和运动性氧去饱和对脂肪组织炎症（ATI）的影响及其对全身性炎症的贡献。设计：对28例临床稳定的COPD患者进行皮下脂肪组织活检研究[1 s用力呼气量：58 +/- 16%预测；BMI（单位：kg/m(2)）： 24.9 +/- 2.9]和15名年龄、性别和身体成分匹配的健康对照受试者。用双能x线吸收仪测量脂肪量。采用增量周期几何法对患者进行氧饱和度预分层。测定脂肪细胞大小和脂肪组织中19个炎症和缺氧相关基因的表达，并对脂肪组织巨噬细胞（ATMs）进行组织学定量。全身炎症标志物包括c反应蛋白（CRP）和一组20种脂肪因子。结果：COPD患者的脂肪量相当，但CRP和HOMA-IR高于对照组。COPD患者和对照组具有相似的脂肪组织基因表达、脂肪细胞大小、ATM浸润和全身脂肪因子浓度。去饱和COPD患者的ATI状态与非去饱和COPD患者没有差异。高CRP COPD患者的ATM浸润明显大于低CRP患者，且与BMI和脂肪质量无关。结论：与匹配良好的健康对照组相比，在COPD患者中，轻至中度COPD本身并不会增强ATI或其对全身性炎症的贡献。然而，据我们所知，我们的研究提供了atm在COPD全身性炎症反应中的可能作用的第一个指示，需要进一步的研究。该试验在www.trialregister.nl注册为NTR1402。m J . clinn [2011]；94: 1504 - 12所示。
Background: Low-grade systemic inflammation is common in chronic obstructive pulmonary disease (COPD), but its source remains unclear. Adipose tissue is a potent producer of inflammatory mediators and may contribute to systemic inflammation in COPD, possibly via hypoxia.Objective: We studied the influence of COPD and exercise-induced oxygen desaturation on adipose tissue inflammation (ATI) and its contribution to systemic inflammation.Design: Subcutaneous adipose tissue biopsies were investigated in 28 clinically stable COPD patients [forced expiratory volume in 1 s: 58 +/- 16% predicted; BMI (in kg/m(2)): 24.9 +/- 2.9] and 15 age-, sex-, and body composition-matched healthy control subjects. Fat mass was measured with dual-energy X-ray absorptiometry. Patients were prestratified by oxygen desaturation assessed by incremental cycle ergometry. The adipocyte size and adipose tissue expression of 19 inflammatory and hypoxia-related genes were measured, and adipose tissue macrophages (ATMs) were histologically quantified. Systemic inflammatory markers included C-reactive protein (CRP) and a panel of 20 adipokines.Results: COPD patients had comparable fat mass but higher CRP and HOMA-IR than did control subjects. COPD patients and control subjects had comparable adipose tissue gene expression, adipocyte size, ATM infiltration, and systemic adipokine concentrations. Desaturating COPD patients had no different ATI status than did non-desaturating COPD patients. COPD patients with high CRP had significantly greater ATM infiltration than did patients with low CRP, which was independent of BMI and fat mass.Conclusions: In COPD patients, mild-to-moderate COPD, per se, does not enhance ATI or its contribution to systemic inflammation compared with in well-matched healthy control subjects. However, to our knowledge, our study provides a first indication for a possible role of ATMs in the systemic inflammatory response in COPD that requires additional investigation. This trial was registered at www.trialregister.nl as NTR1402. Am J Clin Nutr 2011; 94: 1504-12.