Idiopathic pulmonary fibrosis (IPF) is a chronic age-related disease with increasing prevalence that is characterised by progressive loss of lung function, which contributes to accelerated morbidity and mortality. While the exact aetiology is unknown, studies in patients with IPF and murine models of lung fibrosis have established genetic mutations1 2 and telomere dysfunction in alveolar epithelial cells3 as molecular drivers that lead to a series of events involving aberrant repair, fibroblast activation, senescence reprogramming, epithelial to mesenchymal transition and inflammatory cell recruitment to the fibrotic niche. After onset, disease progression is variable, with some patients suffering acute exacerbation. Although the cause of acute exacerbation remains unknown, they may be encountered in patients exposed to secondary insults, such as environmental pollutants like chitin polysaccharides,4 5 smoking and altered immune response.6 To better understand the aetiology of acute exacerbation, several groups investigated the role of microbiome in IPF.7–10 Altered and increased bacterial burden is a common finding across all these studies. Molyneaux et al employed 16S bacterial ribosomal RNA sequencing to show there is increased bacterial burden in IPF lungs compared with control subjects and that patient survival was inversely correlated with bacterial burden.7 In the Correlating Outcomes with biochemical Markers to Estimate Time-progression in IPF (COMET-IPF) study, Han and colleagues found a significant association between relative abundance of Streptococcus and Staphylococcus with IPF disease progression.8 More recently, in a bleomycin model of lung fibrosis, O’Dwyer et al report that lung …

中文翻译：

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微生物组诱导的糖酵解途径是特发性肺纤维化急性加重的先兆吗？

特发性肺纤维化 (IPF) 是一种与年龄相关的慢性疾病，其患病率不断增加，其特征是肺功能进行性丧失，这会导致发病率和死亡率加快。虽然确切的病因尚不清楚，但对 IPF 患者和肺纤维化小鼠模型的研究已经确定基因突变 1 2 和肺泡上皮细胞端粒功能障碍 3 作为分子驱动因素，导致一系列事件，包括异常修复、成纤维细胞活化、衰老重编程、上皮间质转化和炎症细胞募集到纤维化生态位。发病后，疾病进展是可变的，一些患者会出现急性加重。虽然急性加重的原因尚不清楚，但在暴露于继发性损伤的患者中可能会遇到这种情况，例如几丁质多糖等环境污染物、4 5 吸烟和改变的免疫反应。6 为了更好地了解急性加重的病因，几个小组调查了微生物组在 IPF 中的作用。7-10 细菌负荷的改变和增加是所有人的共同发现这些研究。Molyneaux 等人使用 16S 细菌核糖体 RNA 测序表明，与对照组相比，IPF 肺部的细菌负荷增加，并且患者存活率与细菌负荷呈负相关。 7 在与生化标志物相关的结果以估计 IPF 的时间进展（ COMET-IPF) 研究中，Han 及其同事发现链球菌和葡萄球菌的相对丰度与 IPF 疾病进展之间存在显着关联。8 最近，在肺纤维化的博莱霉素模型中，