Relationship of adipokines with immune response and lung function in obese asthmatic and non-asthmatic women.
Relationship of adipokines with immune response and lung function in obese asthmatic and non-asthmatic women.
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DOI：
10.3109/02770903.2011.613507
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发表时间：
2011-10
期刊：
影响因子：
--
通讯作者：
Cohen RI
中科院分区：
文献类型：
--
作者：
Dixon AE;Johnson SE;Griffes LV;Raymond DM;Ramdeo R;Soloveichik A;Suratt BT;Cohen RI
肥胖是哮喘的一个危险因素。小鼠研究表明，脂肪因子瘦素和脂联素影响哮喘反应。本研究的目的是确定与肥胖相关的脂肪因子是否在患有哮喘的肥胖女性中与对照组相比发生了改变，以及与过敏性炎症相关的细胞因子和趋化因子的增加是否相关。我们对哮喘和非哮喘的绝经前肥胖妇女进行了一项横断面研究。参与者回答问卷并进行肺功能测试。收集血清和外周血单核细胞（PBMC）用于细胞因子和脂肪因子的分析。共有22名哮喘女性（平均体重指数40.0 ± 5.1 kg/m2）和20名非哮喘女性（平均体重指数41.3 ± 5.6 kg/m2）参与研究。我们发现哮喘患者和非哮喘患者的血清脂肪因子浓度无差异。血清脂联素与PBMC嗜酸性粒细胞趋化因子（rs = 0.55，p = 0.0003）和RANTES（活化后调节，正常T细胞表达和分泌）（rs = 0.36，p = 0.03）呈正相关，而血清瘦素与PBMC嗜酸性粒细胞趋化因子呈负相关（rs =-0.34，p = 0.04）。血清脂联素与PBMC干扰素-γ呈负相关（rs =-0.41，p = 0.01）。在肥胖症中发生的脂肪因子的紊乱与细胞因子产生的减少相关，这些细胞因子产生通常与肥胖绝经前妇女PBMC中的过敏反应相关。这项研究表明，虽然肥胖哮喘患者可能有Th 2介导的炎症的元素，肥胖脂肪因子紊乱与Th 1，而不是Th 2的偏见。肥胖对过敏性炎症反应具有复杂的影响，可能是哮喘气道疾病发病机制的重要调节因素。
Obesity is a risk factor for asthma. Studies in mice suggest that the adipokines leptin and adiponectin affect asthmatic responses. The purpose of this study was to determine if adipokines associated with obesity are altered in obese women with asthma compared to controls and associated with increased cytokines and chemokines involved in allergic inflammation. We performed a cross-sectional study of asthmatic and non-asthmatic obese premenopausal women. Participants answered questionnaires and performed lung function tests. Serum and peripheral blood mononuclear cells (PBMCs) were collected for analysis of cytokines and adipokines. A total of 22 asthmatic (mean body mass index 40.0 ± 5.1 kg/m) and 20 non-asthmatic women (mean body mass index 41.3 ± 5.6 kg/m2) participated. We found no difference in serum adipokine concentrations between asthmatics and non-asthmatics. Serum adiponectin correlated positively with PBMC eotaxin (rs = 0.55, p = .0003) and RANTES (regulated upon activation, normal T-cell expressed, and secreted) (rs = 0.36, p = .03), whereas serum leptin correlated negatively with PBMC eotaxin (rs = −0.34, p = .04). There was a negative correlation between serum adiponectin and PBMC interferon-γ (rs = −0.41, p = .01). Perturbations of adipokines that occur in obesity were correlated with decreased cytokine production typically associated with allergic responses in PBMC of obese premenopausal women. This study suggests that although obese asthmatics may have elements of Th2-mediated inflammation, adipokine derangements in obesity are associated with Th1 rather than Th2 bias. Obesity has complex effects on allergic inflammation and is likely to be important modifier of the pathogenesis of airway disease in asthma.
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影响因子：
12.4
作者：
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