Abstract
Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) have been defined as events of clinically significant respiratory deterioration with an unidentifiable cause. They carry a significant mortality and morbidity and while their exact pathogenesis remains unclear, the possibility remains that hidden infection may play a role. The aim of this pilot study was to determine whether changes in the respiratory microbiota occur during an AE-IPF. Bacterial DNA was extracted from bronchoalveolar lavage from patients with stable IPF and those experiencing an AE-IPF. A hyper-variable region of the 16S ribosomal RNA gene (16S rRNA) was amplified, quantified and pyrosequenced. Culture independent techniques demonstrate AE-IPF is associated with an increased BAL bacterial burden compared to stable disease and highlight shifts in the composition of the respiratory microbiota during an AE-IPF.
Highlights
Current diagnostic criteria for acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) clearly distinguish them from exacerbations of other respiratory diseases [1]
There are a number of factors supporting a role for infection; i) seasonal patterns exist with increased Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) occurring during the winter months, ii) respiratory tract infections in individuals with IPF confer a mortality risk indistinguishable from that seen with acute exacerbations [4], iii) post mortem examination in cases of confirmed infection frequently discloses diffuse alveolar damage identical to that seen
In summary differences in specific Operational Taxonomic Units (OTUs) and bacterial burden suggest that bacteria may play a causative role in some AE-IPF
Summary
Current diagnostic criteria for acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) clearly distinguish them from exacerbations of other respiratory diseases [1]. The exact pathogenesis, remains unknown and it is currently unclear whether AE-IPF represent an accelerated phase of the underlying fibroproliferative process or an exaggerated lung injury response to unidentified preceding or coexistent infection [3]. While the role of viruses in AE-IPF has been extensively investigated [7] there has been little focus on a potential role for bacteria, despite recent evidence that bacterial burden is increased in the IPF lung and changes in the microbiome relate to disease outcomes [8, 9]. In order to explore changes in the bronchoalveolar lavage (BAL) microbiota during an AE-IPF, 16S rRNA gene qPCR and pyrosequencing were performed on both stable and exacerbation samples in subjects with IPF
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