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囊性纤维化肺病中的抗炎细胞因子

Anti-inflammatory cytokines in cystic fibrosis lung disease.

作者信息

Starosta V, Ratjen F, Rietschel E, Paul K, Griese M

机构信息

Lung Research Group, Children's Hospital of Ludwig Maximilians University, Munich, Germany.

出版信息

Eur Respir J. 2006 Sep;28(3):581-7. doi: 10.1183/09031936.06.00071405. Epub 2006 Jun 28.

DOI:10.1183/09031936.06.00071405
PMID:16807263
Abstract

Lung inflammation plays a pivotal role in the pathogenesis of airway disease in cystic fibrosis (CF). An imbalance between pro- and anti-inflammatory mediators has been observed and a deficiency in the anti-inflammatory response has been proposed, but this concept remains controversial. In the present study, the concentrations of two anti-inflammatory mediators, lipoxin A (LxA4) and Clara cell protein 10 (CC-10), were assessed in bronchoalveolar lavage fluid (BALF) of CF patients with a wide range of endobronchial inflammation and disease controls with neutrophilic inflammation unrelated to CF. No differences were observed in LxA4 BALF concentrations between CF patients and controls with a similar degree of neutrophilic airway inflammation. Concentrations were also similar in CF patients with mild versus more severe airway inflammation. In contrast, CC-10 concentrations were lower in CF patients, but this decrease was limited to patients with more intense airway inflammation. The present data do not support the concept of a primary defect in anti-inflammatory mediators in cystic fibrosis lung disease. Although Clara cell protein concentrations were found to be reduced, these alterations appear to be secondary to neutrophilic airway inflammation rather than due to a primary deficiency.

摘要

肺部炎症在囊性纤维化(CF)气道疾病的发病机制中起关键作用。已观察到促炎和抗炎介质之间存在失衡,并有人提出抗炎反应存在缺陷,但这一概念仍存在争议。在本研究中,对一系列支气管内炎症程度不同的CF患者的支气管肺泡灌洗液(BALF)以及患有与CF无关的嗜中性粒细胞性炎症的疾病对照组,评估了两种抗炎介质脂氧素A(LxA4)和克拉拉细胞蛋白10(CC-10)的浓度。在嗜中性气道炎症程度相似的CF患者和对照组之间,未观察到LxA4 BALF浓度的差异。轻度与更严重气道炎症的CF患者的浓度也相似。相比之下,CF患者的CC-10浓度较低,但这种降低仅限于气道炎症更严重的患者。目前的数据不支持囊性纤维化肺病中抗炎介质存在原发性缺陷的概念。尽管发现克拉拉细胞蛋白浓度降低,但这些改变似乎是嗜中性气道炎症的继发结果,而非原发性缺陷所致。

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