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Down‐regulated surfactant protein B in obese asthmatics

机译:肥胖哮喘患者中下调表面活性剂蛋白B

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Abstract Background Obesity is a common comorbid condition in adult asthmatics and known as a feature of asthma severity. However, the molecular mechanism under obesity‐induced inflammation has not yet been fully understood. Objective Considering the essential role of hydrophobic surfactant protein B (SP‐B) in lung function, SP‐B was targeted to examine its involvement in the development of obesity‐induced airway inflammation in asthmatics. Methods The aim was to examine an alteration in circulating SP‐B according to obesity in adult asthmatics, 129 asthmatics were enrolled and classified into 3?groups (obese, overweight and normal‐weight groups) according to body mass index (BMI). Circulating SP‐B levels were determined by enzyme‐linked immunosorbent assay. Four single nucleotide polymorphisms of SFTPB gene were genotyped. Serum ceramide levels were measured by liquid chromatography‐tandem mass spectrometry. Results Significantly lower serum SP‐B levels were noted in the obese group than in the overweight or normal‐weight group (p?=?.002). The serum SP‐B level was significantly correlated with serum levels of C18:0 ceramide and transforming growth factor beta?1 as well as BMI (r?=??0.200; r?=??0.215; r?=??0.332, p?G to the obese and overweight groups was noted. Conclusion Obesity altered ceramide metabolism leading to pulmonary surfactant dysfunction and impaired?resolution of airway inflammation, finally contributing to the phenotypes of obese asthmatics.
机译:摘要 背景 肥胖是成人哮喘患者常见的合并症,是哮喘严重程度的一个特征。然而,肥胖诱导炎症的分子机制尚未完全了解。目的 探讨疏水性表面活性蛋白B(SP-B)在肺功能中的重要作用,靶向研究SP-B参与哮喘患者肥胖诱导的气道炎症发展。方法 研究成人哮喘患者肥胖情况对循环SP-B的改变,选取129例哮喘患者为研究对象,根据体重指数(BMI)分为3组(肥胖组、超重组和正常体重组)。循环SP-B水平通过酶联免疫吸附测定法测定。对SFTPB基因的4个单核苷酸多态性进行基因分型。通过液相色谱-串联质谱法测定血清神经酰胺水平。结果 肥胖组血清SP-B水平明显低于超重组或正常体重组(p?=?。002)血清SP-B水平与血清C18:0神经酰胺和转化生长因子β?1水平以及BMI(r?=??0.200;r?=??0.215;r?=??0.332,页?。050 为所有人)。女性哮喘患者的血清SP-B与呼出气一氧化氮水平呈负相关(r?=??0.287,p?=?。009). 注意到 9306 A>G 的 SFTPB 基因对肥胖和超重组的遗传易感性。结论 肥胖改变神经酰胺代谢导致肺表面活性物质功能障碍和气道炎症消退受损,最终导致肥胖哮喘患者的表型。

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