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感染在特发性肺纤维化发病机制中的作用。

The role of infection in the pathogenesis of idiopathic pulmonary fibrosis.

机构信息

Dept of Respiratory Medicine, Royal Brompton Hospital, London, UK.

出版信息

Eur Respir Rev. 2013 Sep 1;22(129):376-81. doi: 10.1183/09059180.00000713.

DOI:10.1183/09059180.00000713
PMID:23997064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9487348/
Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive, and invariably fatal, condition that is believed to arise in genetically susceptible individuals as a consequence of an aberrant wound-healing response following repetitive alveolar injury. The exact triggers, which initiate the fibrotic process, remain unknown. Infectious agents, including both viruses and bacteria, have the capacity to cause alveolar-epithelial cell injury and apoptosis. Relatively few studies have examined the role of infection in IPF. Those that have, point to viruses playing a key role as cofactors in the initiation and progression of IPF. There is also some evidence to suggest that viral infection may be responsible for a proportion of acute exacerbations of IPF. The role played by bacteria in the pathogenesis of IPF is less clear cut. Studies from other respiratory diseases suggest that alterations in the lung microbiome are associated with disease and that these changes influence disease behaviour. Emerging molecular microbiological techniques are making the study of microbial communities in the lung easier. It is hoped that by combining such techniques with the careful longitudinal phenotyping of patients with IPF, it will be possible to elucidate the role played by bacteria and viruses in the pathogenesis of the disease. If infection plays a causal role in IPF then it is possible that therapeutic strategies, utilising currently available antiviral or antibiotic drugs, may be effective in modifying the course of this devastating condition.

摘要

特发性肺纤维化(IPF)是一种进行性且不可避免的致命疾病,据信它是由于遗传易感个体在反复的肺泡损伤后发生异常的伤口愈合反应而引起的。确切的触发因素,即启动纤维化过程的因素,仍然未知。感染因子,包括病毒和细菌,都有能力引起肺泡上皮细胞损伤和细胞凋亡。相对较少的研究检查了感染在 IPF 中的作用。那些研究表明,病毒作为 IPF 起始和进展的协同因素起着关键作用。还有一些证据表明,病毒感染可能导致一部分 IPF 的急性加重。细菌在 IPF 发病机制中的作用不太明确。来自其他呼吸系统疾病的研究表明,肺部微生物组的改变与疾病有关,这些变化影响疾病的行为。新兴的分子微生物学技术使研究肺部微生物群落变得更加容易。人们希望通过将这些技术与对 IPF 患者进行仔细的纵向表型分析相结合,有可能阐明细菌和病毒在疾病发病机制中的作用。如果感染在 IPF 中起因果作用,那么利用现有抗病毒或抗生素药物的治疗策略可能有效改变这种破坏性疾病的进程。

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