Angiogenic and Angiostatic Chemokines in Idiopathic Pulmonary Fibrosis and Granulomatous Lung Disease
Angiogenic and Angiostatic Chemokines in Idiopathic Pulmonary Fibrosis and Granulomatous Lung Disease
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DOI：
10.1159/000245332
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发表时间：
2010-01-01
期刊：
影响因子：
3.7
通讯作者：
Costabel, Ulrich
中科院分区：
文献类型：
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作者：
Cui, Ai;Anhenn, Olaf;Costabel, Ulrich
背景：不同浓度的趋化因子影响血管生成-血管抑制平衡和白细胞募集。目的：为了研究血管生成性和血管抑制性CXC趋化因子对特发性肺纤维化（IPF）和肉芽肿性肺病发病机制的相对贡献，我们检测了肺泡巨噬细胞体外产生的血管生成性趋化因子（IL-8）和2种血管抑制性趋化因子（IP-10和IL-8）。研究方法：将16例肉芽肿性肺病患者[8例结节病患者，8例外源性过敏性肺泡炎（EAA）患者]、16例IPF患者和8例对照受试者的肺泡巨噬细胞培养24 h。通过基于荧光珠的多重技术测量培养上清液中的IL-8、IL-18、IP-10和IL-18。结果如下：在IPF患者中，IL-8升高并与支气管肺泡灌洗（BAL）中性粒细胞相关，而IP-10和IL-10水平正常。在结节病和EAA患者中，IL-8、IP-10和IL-10均升高，IP-10和IL-10与IL-18（一种Th 1细胞因子）以及BAL淋巴细胞的百分比和数量相关。结论：CXC趋化因子和Th 1细胞因子表达的差异可能导致这些疾病的不同免疫发病机制、临床病程和对治疗的反应性。版权所有（C）2009 S. Karger AG，巴塞尔
Background: Angiogenesis-angiostasis balance and leukocyte recruitment are influenced by different concentrations of distinct chemokines. Objective: To investigate the relative contribution of angiogenic and angiostatic CXC chemokines to the pathogenesis of idiopathic pulmonary fibrosis (IPF) and granulomatous lung diseases, we examined the in vitro production of an angiogenic chemokine (IL-8), and 2 angiostatic chemokines (IP-10 and MIG) by alveolar macrophages. Methods: Alveolar macrophages from 16 patients with granulomatous lung diseases [8 with sarcoidosis, 8 with extrinsic allergic alveolitis (EAA)], 16 patients with IPF, and 8 control subjects were cultured for 24 h. IL-8, IL-18, IP-10 and MIG in the culture supernatants were measured by a fluorescent bead-based multiplex technique. Results: In IPF patients, IL-8 was increased and correlated with bronchoalveolar lavage (BAL) neutrophils, whereas the levels of IP-10 and MIG were normal. In sarcoidosis and EAA patients, IL-8, IP-10, and MIG were all increased and IP-10 and MIG correlated with IL-18, a Th1 cytokine, and the percentage and number of BAL lymphocytes. Conclusions: The difference in the expression of CXC chemokines and a Th1 cytokine may contribute to the different immunopathogenesis, clinical course and responsiveness to treatment of these diseases. Copyright (C) 2009 S. Karger AG, Basel