Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Clin Exp Allergy. 2022 Nov;52(11):1321-1329. doi: 10.1111/cea.14124. Epub 2022 Mar 22.
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.
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.
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.
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 < .050 for all). An inverse correlation was noted between serum SP-B and fractional exhaled nitric oxide levels in female asthmatics (r = -0.287, p = .009). Genetic predisposition of the SFTPB gene at 9306 A>G to the obese and overweight groups was noted.
Obesity altered ceramide metabolism leading to pulmonary surfactant dysfunction and impaired resolution of airway inflammation, finally contributing to the phenotypes of obese asthmatics.
肥胖是成年哮喘患者常见的合并症，也是哮喘严重程度的特征之一。然而，肥胖引起的炎症的分子机制尚未完全阐明。
考虑到疏水性表面活性蛋白 B (SP-B) 在肺功能中的重要作用，本研究旨在研究 SP-B 在肥胖诱导的哮喘患者气道炎症发展中的作用。
本研究旨在检测肥胖对成年哮喘患者循环 SP-B 的影响，共纳入 129 名哮喘患者，并根据体重指数 (BMI) 将其分为 3 组（肥胖组、超重组和正常体重组）。通过酶联免疫吸附试验测定循环 SP-B 水平。对 SFTPB 基因的 4 个单核苷酸多态性进行基因分型。采用液相色谱-串联质谱法测定血清神经酰胺水平。
与超重或正常体重组相比，肥胖组患者血清 SP-B 水平显著降低（p = 0.002）。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 呈显著负相关（r = -0.200；r = -0.215；r = -0.332，均 p < 0.050）。女性哮喘患者中，血清 SP-B 与呼出气一氧化氮分数呈负相关（r = -0.287，p = 0.009）。SFTPB 基因 9306 A>G 多态性与肥胖和超重组有关。
肥胖改变了神经酰胺代谢，导致肺表面活性物质功能障碍和气道炎症消退受损，最终导致肥胖型哮喘患者的表型。
