The Role of the Lung's Microbiome in the Pathogenesis and Progression of Idiopathic Pulmonary Fibrosis.
acute exacerbation
idiopathic pulmonary fibrosis
infection
interstitial lung disease
microbiome
pathogenesis
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
10 Nov 2019
10 Nov 2019
Historique:
received:
22
10
2019
revised:
04
11
2019
accepted:
08
11
2019
entrez:
14
11
2019
pubmed:
14
11
2019
medline:
14
4
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 31717661
pii: ijms20225618
doi: 10.3390/ijms20225618
pmc: PMC6888416
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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