IL-33与原发干燥综合征肺间质病变和肺功能相关性分析
| 作者: |
1段利华,
1石桂秀
1 厦门大学附属第一医院风湿免疫科，福建 厦门 361003 |
| 通讯: |
段利华
Email: lh-duan@163.com |
| DOI: | 10.3978/j.issn.2095-6959.2015.12.013 |
| 基金: | 国家自然科学基金项目资助, 81302564 |
摘要
目的：研究IL-33与原发性干燥综合征(primary sjogren’s syndrome，pSS)并发肺间质病变(interstitiallung disease，ILD)以及肺功能的相关性分析。方法：收集73例原发性干燥综合征新确诊患者，HRCT评估肺部间质性改变，其中31例患者存在间质性改变，42例无间质性肺炎改变。募集31例健康志愿者。测定患者和健康志愿者的肺功能。收集患者和健康志愿者外周血血清，ELISA检测血清中IL-33的表达。肺功能仪器检测用力肺活量(forced vital capacity，FVC)、第1秒用力呼气容积(forced expiratory volume in 1 second，FEV1)、一氧化碳弥散功能(diffusing capacity for carbonmonoxide ，DLco)。统计分析IL-33与肺功能指标的关系。结果：pSS患者血清IL-33表达均显著高于正常健康对照组(P<0.001)。pSS合并肺间质病变患者(pSS-ILD)与pSS无肺间质性病变患者(pSSnoILD)的IL-33表达，均高于正常对照组。pSS-ILD与pSS-no ILD相比，IL-33在pSS-ILD表达显著升高(P<0.05)，且与肺功能指标DLco呈负相关(r=−0.42，P=0.02)。结论：IL-33可能参与了原发性干燥综合征肺间质病变病理过程，并影响肺弥散功能改变。
关键词：
IL-33
干燥综合征
肺间质病变
Contribution of interleukin-33 on the development of interstitial lung disease in primary sjogren’s syndrome
CorrespondingAuthor: DUAN Lihua Email: lh-duan@163.com
DOI: 10.3978/j.issn.2095-6959.2015.12.013
Abstract
Objective: To analyze the correlation of interleukin-33 (IL-33) with interstitial lung disease (ILD) and pulmonary function in the primary sjogren’s syndrome (pSS) patients. Methods: A total of 73 new pSS patients and 31 healthy control subject were collected. HRCT of the chest and pulmonary function testing tests (PFTs) were performed to assess radiographic and functional abnormalities indicative of ILD. The 31 patients had evidence of definite interstitial lung abnormalities on chest HRCT. The sera IL-33 expression in patients and controls was detected by ELISA. In addition, the forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), and diffusing capacity for carbon monoxide (DLco) (FVC) were evaluated. The correlations between IL-33 and above clinical parameters were analyzed. Results: The levels of IL-33 in pSS patients and healthy volunteers were analyzed. As compared with healthy control, pSS patients showed a high level of IL-33 (P<0.001). The expression of IL-33 in pSS patients with or without interstitial lung disease were both significantly higher than healthy control. Furthermore, a markedly increase IL-33 expression were observed in pSS with interstitial lung disease (pSS-ILD) when compared with no interstitial lung disease in pSS (pSS-no ILD) (P<0.05). Interestingly, in the pSS with interstitial lung disease (pSS-ILD) group, a significant correlations between the expression of IL-33 and parameters of pulmonary function testing tests was observed(r=−0.42, P=0.02). Conclusion: IL-33 might involves in the pathogenesis of sjogren’s syndrome associated interstitial lung disease, therefore result in reducing the diffusing capacity of pulmonary function.