哮喘联盟

   摘要
   目的：研究白介素33（IL-33）在哮喘患者气道重塑过程的作用，并研究其与哮喘严重程度的关系。
   方法：对45例哮喘患者及40例非过敏性正常对照组受试者检测以下指标：IL-33水平、痰液嗜酸性细胞百分比（EOS%）、肺功能及总IgE水平，并评估哮喘患者的严重程度。采用苏木精伊红染色法（HE法）及免疫组织化学染色，对8例哮喘患者及8例非过敏性正常对照的支气管活检标本检测IL-33的表达水平及网状基底膜（RBM）的厚度。在体外，通过实时荧光PCR以及免疫印迹法鉴定IL-33的特殊作用。
   结果：哮喘患者血清IL-33水平高于非过敏性正常对照。另外，在哮喘患者中，血清IL-33水平与第1秒用力呼气量（FEV1，占预计值百分比）呈负相关，而与哮喘患者的严重程度呈正相关。在哮喘患者的支气管活检标本中检测到IL-33表达量增加以及RBM增厚。患者血清IL-33水平与网状基底膜厚度呈正相关。体外用IL-33处理24小时后，人肺成纤维细胞（HLF-1）纤连蛋白及I型胶原蛋白的合成量增加。预先给予抗ST2抗体或氟替卡松丙酸酯（FP）处理可抑制IL-33诱导的纤连蛋白及I型胶原合成。
   结论：IL-33可作为哮喘严重程度的生物指标。同时，它还可能通过作用于人肺成纤维细胞有助于哮喘患者气道重塑。

 

（刘国梁 审校）
J Asthma. 2014 May 6. [Epub ahead of print]

 

IL-33 promotes airway remodeling and is a marker of asthma disease severity.
 

Guo Z1, Wu J, Zhao J, Liu F, Chen Y, Bi L, Dong L, Liu S.
 

ABSTRACT
OBJECTIVE: To investigate the function of interleukin-33 (IL-33) in the asthmatic airway remodeling and the relationship between IL-33 and asthma severity.
METHODS: IL-33 levels, sputum eosinophils percentage (EOS%), pulmonary function and total immunoglobulin (IgE) were measured for 45 patients with asthma and 40 non-allergic controls. Asthma severity was assessed. The expressions of IL-33 and reticular basement membrane (RBM) on bronchial biopsy specimens from 8 asthma patients and 8 non-allergic controls were observed after hematoxylin-eosin staining(HE) and immunohistochemical staining. In vitro experiments, real-time polymerase chain reactions and western blotting analysis were used to identify the specific effects of IL-33 administration.
RESULTS:Serum IL-33 levels in patients with asthma were higher than those in non-allergic controls. Moreover, in asthmatic patients, serum IL-33 levels were negatively correlated to forced expiratory volume in one second (FEV1, % predicted), and positively correlated to asthma severity. Increased expression of IL-33 and RBM thickening were observed on bronchial biopsy specimens obtained from patients with asthma. Serum IL-33 levels were positively correlated to basement membrane thickness. The production of fibronectin1 and type I collagen in human lung fibroblasts (HLF-1) increased at 24 h after IL-33 treatment in vitro. Pre-treatment with anti-ST2 antibody or fluticasone propionate (FP) suppressed the production of fibronectin1 and types I collagen induced by IL-33.
CONCLUSIONS: IL-33 is a marker of asthma severity, and may contribute to airway remodeling in asthma by acting on human lung fibroblasts.
 

J Asthma. 2014 May 6. [Epub ahead of print]