TABLE 2

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

Diagnosis	Main conclusions	[Ref.]
IPF	Positive 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	[37]
AE-IPF	Four-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	[38]
	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.