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Humankind’s greatest enemy has always been, and likely will always be, infection. The role of infection in idiopathic pulmonary fibrosis (IPF) is a poorly understood but the emergence of molecular techniques has renewed the focus on this area. Earlier studies of histological sections identified herpes virus DNA and haemophilus species in lung tissue.1 More recently, studies have used high sensitivity and high throughput techniques to assess bacterial species in bronchoavleoar lavage (BAL). A large number of studies have now identified divergent bacterial species in the BAL and have associated them with mechanistic processes that give biological plausibility to the role of luminal infections promoting the development of IPF.2–4
It is therefore somewhat surprising that in the study by …
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