摘要
肺囊性纤维化肺部疾病的特点是慢性、非解决先天免疫系统的激活和过度释放细胞因子及趋化因子如IL-8和免疫细胞,主要是中性粒细胞持续浸润,进入呼吸道。慢性感染和受损的免疫反应,最终导致肺损伤的特点是支气管扩张、肺气肿、肺纤维化。作为一个完整解释在肺纤维化疾病的夸张的炎症反应的知识的途径是缺乏的,了解这些途径可以揭示新的治疗目标,并引领新的治疗。因此,此处有一个强有力的理由鉴定在肺疾病的机制和途径下夸张的炎症反应。本文综述了炎症的肺囊性纤维化肺部疾病的发病机制中的作用,对异常信号参与趋化因子IL-8和肺囊性纤维化航空公司招募中性粒细胞过度表达的重点。研究结果表明,针对在免疫细胞信号传导通路(尤其是中性粒细胞)夸张的IL-8/IL-8受体(主要是CXCR2)可能代表了肺囊性纤维化肺部疾病的一种潜在的治疗策略。
关键词: 囊性纤维化,肺部炎症、CFTR,趋化因子信号,IL-8,CXCR2,NF-κB。
Current Drug Targets
Title:Dysregulated Chemokine Signaling in Cystic Fibrosis Lung Disease: A Potential Therapeutic Target
Volume: 17 Issue: 13
Author(s): Xiaoqing Guan, Yuning Hou, Fei Sun, Zhe Yang, Chunying Li
Affiliation:
关键词: 囊性纤维化,肺部炎症、CFTR,趋化因子信号,IL-8,CXCR2,NF-κB。
摘要: CF lung disease is characterized by a chronic and non-resolving activation of the innate immune system with excessive release of chemokines/cytokines including IL-8 and persistent infiltration of immune cells, mainly neutrophils, into the airways. Chronic infection and impaired immune response eventually lead to pulmonary damage characterized by bronchiectasis, emphysema, and lung fibrosis. As a complete knowledge of the pathways responsible for the exaggerated inflammatory response in CF lung disease is lacking, understanding these pathways could reveal new therapeutic targets, and lead to novel treatments. Therefore, there is a strong rationale for the identification of mechanisms and pathways underlying the exaggerated inflammatory response in CF lung disease. This article reviews the role of inflammation in the pathogenesis of CF lung disease, with a focus on the dysregulated signaling involved in the overexpression of chemokine IL-8 and excessive recruitment of neutrophils in CF airways. The findings suggest that targeting the exaggerated IL-8/IL-8 receptor (mainly CXCR2) signaling pathway in immune cells (especially neutrophils) may represent a potential therapeutic strategy for CF lung disease.
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Cite this article as:
Xiaoqing Guan, Yuning Hou, Fei Sun, Zhe Yang, Chunying Li , Dysregulated Chemokine Signaling in Cystic Fibrosis Lung Disease: A Potential Therapeutic Target, Current Drug Targets 2016; 17 (13) . https://dx.doi.org/10.2174/1389450117666151209120516
DOI https://dx.doi.org/10.2174/1389450117666151209120516 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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