Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease that commonly affects older adults and is associated with the histopathological and/or radiological patterns of usual interstitial pneumonia (UIP). Despite significant advances in our understanding of disease pathobiology and natural history, what causes IPF remains unknown. A potential role for infection in the disease’s pathogenesis and progression or as a trigger of acute exacerbation has long been postulated, but initial studies based on traditional culture methods have yielded inconsistent results. The recent application to IPF of culture-independent techniques for microbiological analysis has revealed previously unappreciated alterations of the lung microbiome, as well as an increased bacterial burden in the bronchoalveolar lavage (BAL) of IPF patients, although correlation does not necessarily entail causation. In addition, the lung microbiome remains only partially characterized and further research should investigate organisms other than bacteria and viruses, including fungi. The clarification of the role of the microbiome in the pathogenesis and progression of IPF may potentially allow its manipulation, providing an opportunity for targeted therapeutic intervention.
Highlights
The term “microbiome” refers to the “ecological community of commensal, symbiotic and pathogenic organisms that share our body space,” [1] as well as the complex interactions of these microbes with the host
We summarize and critically discuss current knowledge about the interplay between the lung microbiome and Idiopathic pulmonary fibrosis (IPF), with emphasis on its potential role in disease development, progression and acute exacerbation
The limitations of the animal models of IPF notwithstanding, this study provides a potential mechanistic link between lung bacterial burden and disease pathogenesis and progression in pulmonary fibrosis
Summary
The term “microbiome” refers to the “ecological community of commensal, symbiotic and pathogenic organisms that share our body space,” [1] as well as the complex interactions of these microbes with the host. The gastrointestinal microbiome, composed of more than 100 trillion microorganisms, is the most extensively studied [2]; the epithelial surface of the lower respiratory tract, one of the least populated surfaces of the human body, has historically been described as sterile. This incorrectly held doctrine arose primarily because of the challenge of directly sampling the lower airways and the limitations of bacterial culture, which prevented isolation and identification of microbes. We summarize and critically discuss current knowledge about the interplay between the lung microbiome and IPF, with emphasis on its potential role in disease development, progression and acute exacerbation
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