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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 …
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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