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The first line of defence in the airways is the epithelium. In health there are numerous mechanisms to repel invaders and facilitate repair of this barrier. However, when these mechanisms are ineffective, absent or simply become exhausted, fibrosis can ensue.1 For many years epidemiological studies have highlighted potential environmental triggers which could target and damage the epithelium in idiopathic pulmonary fibrosis (IPF), but more recently we have come to understand the role of bacteria, and specifically the role of the ever-present respiratory microbiota in fibrogenesis.
The dysbiosis of the lower airway microbiota in IPF has now been well described. There are clear associations with both the content and quantity of bacteria and clinical disease behaviour, with the most consistent signal related to the overall bacterial burden.2–5 This relationship is not simply the result of extensive anatomical changes or related to the extent of fibrosis6 and is specific to IPF.7 However, the potential mechanisms by …
Contributors PLM wrote manuscript.
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 PLM, via his institution, received industry-academic funding from AstraZeneca and has received speaker and consultancy fees from Boehringer Ingelheim and Hoffmann-La Roche, outside the submitted work.
Patient consent for publication Not required.
Provenance and peer review Commissioned; externally peer reviewed.
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