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哮喘与肥胖中的脂联素:是保护因子还是更严重疾病的危险因素?

Adiponectin in Asthma and Obesity: Protective Agent or Risk Factor for More Severe Disease?

作者信息

de Lima Azambuja Renato, da Costa Santos Azambuja Layla Salomao Eulalio, Costa Cláudia, Rufino Rogério

机构信息

Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, CEP 20551-030, Brazil.

Pulmonology Department, Hospital Universitário Pedro Ernesto, Avenida 28 de Setembro, 77, Rio de Janeiro, RJ, CEP 20551-030, Brazil.

出版信息

Lung. 2015 Oct;193(5):749-55. doi: 10.1007/s00408-015-9793-8. Epub 2015 Aug 28.

Abstract

PURPOSE

The relationship between asthma and obesity is well established, although the pathophysiological mechanisms linking both diseases remain unknown. Adiponectin is a hormone secreted by adipose cells, plays a role in the modulation of inflammation and may be the key linking these two types of inflammation.

METHODS

We conducted a cross-sectional study with asthma with different body mass indices (BMI); the patients were classified as eutrophic, overweight, or obese. We assessed disease control using the GINA consensus, and the levels of adiponectin, C-reactive protein (CRP) and interleukin 33 (IL-33) in each of the patients.

RESULTS

We evaluated 75 of the 96 patients eligible for the study, including 25 in each BMI group. The CRP levels were significantly higher in the obese patients compared with both the eutrophic (p = 0.01) and the overweight (p = 0.03) patients. The mean adiponectin level was 21.82 ± 9.93 mg/L for the eutrophic asthmatics, which is a level that was significantly higher than in the overweight (15.31 ± 6.27 mg/L, p = 0.0140) and the obese (16.69 ± 11.45 mg/L, p = 0.0287) patients. The patients with higher adiponectin levels exhibited smaller FEV1 (p = 0.02) and lower FVC (p = 0.003). The IL-33 levels were not different between the groups.

CONCLUSIONS

Adiponectin does not protect against the development of inflammation in the setting of asthma and may in fact exacerbate the disease via its anti-TH1 inflammatory effects, allowing for increased TH2 differentiation and a more severe allergic response.

摘要

目的

哮喘与肥胖之间的关系已得到充分证实,尽管将这两种疾病联系起来的病理生理机制仍不清楚。脂联素是一种由脂肪细胞分泌的激素,在炎症调节中发挥作用,可能是连接这两种炎症的关键因素。

方法

我们对不同体重指数(BMI)的哮喘患者进行了一项横断面研究;患者被分为营养正常、超重或肥胖。我们使用全球哮喘防治创议(GINA)共识评估疾病控制情况,并检测每位患者的脂联素、C反应蛋白(CRP)和白细胞介素33(IL-33)水平。

结果

我们评估了96名符合研究条件的患者中的75名,每个BMI组各25名。与营养正常(p = 0.01)和超重(p = 0.03)患者相比,肥胖患者的CRP水平显著更高。营养正常的哮喘患者脂联素平均水平为21.82±9.93mg/L,这一水平显著高于超重(15.31±6.27mg/L,p = 0.0140)和肥胖(16.69±11.45mg/L,p = 0.0287)患者。脂联素水平较高的患者FEV1较小(p = 0.02),FVC较低(p = 0.003)。各组间IL-33水平无差异。

结论

在哮喘情况下,脂联素并不能预防炎症的发生,事实上可能通过其抗TH1炎症作用加剧疾病,使TH2分化增加,过敏反应更严重。

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