Summary of studies linking the respiratory microbiome with the pathogenesis, progression and acute exacerbation of idiopathic pulmonary fibrosis (IPF)

DiagnosisMain conclusions[Ref.]
IPFPositive BAL cultures in eight out of 22 stable IPF subjects: Haemophilus influenzae (n=2), Haemophilus parainfluenzae (n=2), Moraxella catarrhalis (n=1), Pseudomonas aeruginosa (n=1), Proteus mirabilis (n=1), Streptococcus pneumonia (n=1)[33]
Increased abundance of Streptococcus OTU1345 and Staphylococcus OTU1348 is associated with a significant reduction in progression-free survival in IPF[34]
Streptococcus pneumoniae triggers progression of pulmonary fibrosis through pneumolysin in two different mouse models[35]
Increased bacterial burden in IPF subjects compared with COPD and healthy controls[36]
Higher bacterial burden at the time of diagnosis predicts disease progression in IPF[37]
Germ-free mice protected from mortality following bleomycin exposure
AE-IPFFour-fold increase in bacterial burden in AE-IPF subjects compared to stable IPF[38]
Increased abundance of Campylobacter and Stenotrophomonas and decreased abundance of Veillonella in AE-IPF compared to stable IPF
Positive sputum cultures in nine out of 48 AE-IPF subjects: Klebsiella pneumoniae (n=2), Mycobacterium tuberculosis (n=4), Pseudomonas aeruginosa (n=1), Loffi Acinetobacter (n=1), other (n=1)[29]

AE-IPF: acute exacerbation of IPF; BAL: bronchoalveolar lavage.