The contribution of infection and the respiratory microbiome in acute exacerbations of idiopathic pulmonary fibrosis

Rachele Invernizzi; Philip L. Molyneaux

doi:10.1183/16000617.0045-2019

Tables

TABLE 1

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

Virus	Main conclusions	[Ref.]
HHV	EBV detected in serum of 12 out of 13 subjects with IPF but not in patients with other forms of ILD	[22]
	MHV-68 triggers an exaggerated fibrotic response in mice	[23]
	Increased incidence of EBV in BAL and lung biopsies of IPF subjects compared to controls	[24, 25]
	EBV detected in BAL of two out of 43 AE-IPF subjects	[26]
	CMV detected in BAL of two out of 43 AE-IPF subjects	[27]
	A total of 38% of AE-IPF subjects exhibited evidence of CMV infection	[28]
	HHV detected in nasopharyngeal swabs of 15 out of 30 AE-IPF subjects and four out of 30 individuals with stable IPF	[29]
TTV	TTV detected in BAL of 12 out of 43 AE-IPF subjects	[26]
	No evidence of TTV in BAL of stable IPF subjects	[30]
	Increased mortality in IPF subjects with presence of TTV-DNA in serum compared to IPF subjects with no TTV-DNA	[30]
Influenza A	Influenza A detected in nasopharyngeal swabs of 12 out of 30 AE-IPF subjects but not in individuals with stable IPF	[29]
	A case of AE-IPF was reported following pandemic influenza A vaccination	[31]

HHV: human herpes virus; TTV: torque teno virus; EBV: Epstein–Barr virus; ILD: interstitial lung disease; MHV-68: murine γherpes virus-68; BAL: bronchoalveolar lavage; AE-IPF: acute exacerbation of IPF; CMV: cytomegalovirus.

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]