The Respiratory Microbiome in Chronic Hypersensitivity Pneumonitis Is Distinct from That of Idiopathic Pulmonary Fibrosis

: Chronic hypersensitivity pneumonitis (CHP) is a condition that arises after repeated exposure and sensitization to inhaled antigens. The lung microbiome is increasingly implicated in respiratory disease, but, to date, no study has investigated the composition of microbial communities in the lower...

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Published inAmerican journal of respiratory and critical care medicine Vol. 203; no. 3; pp. 339 - 347
Main Authors Invernizzi, Rachele, Wu, Benjamin G., Barnett, Joseph, Ghai, Poonam, Kingston, Shaun, Hewitt, Richard J., Feary, Johanna, Li, Yonghua, Chua, Felix, Wu, Zhe, Wells, Athol U., George, Peter M., Renzoni, Elisabetta A., Nicholson, Andrew G., Rice, Alexandra, Devaraj, Anand, Segal, Leopoldo N., Byrne, Adam J., Maher, Toby M., Lloyd, Clare M., Molyneaux, Philip L.
Format Journal Article
LanguageEnglish
Published United States American Thoracic Society 01.02.2021
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Summary:: Chronic hypersensitivity pneumonitis (CHP) is a condition that arises after repeated exposure and sensitization to inhaled antigens. The lung microbiome is increasingly implicated in respiratory disease, but, to date, no study has investigated the composition of microbial communities in the lower airways in CHP. To characterize and compare the airway microbiome in subjects with CHP, subjects with idiopathic pulmonary fibrosis (IPF), and control subjects. We prospectively recruited individuals with a CHP diagnosis (  = 110), individuals with an IPF diagnosis (  = 45), and control subjects (  = 28). Subjects underwent BAL and bacterial DNA was isolated, quantified by quantitative PCR and the 16S ribosomal RNA gene was sequenced to characterize the bacterial communities in the lower airways. Distinct differences in the microbial profiles were evident in the lower airways of subjects with CHP and IPF. At the phylum level, the prevailing microbiota of both subjects with IPF and subjects with CHP included , , , and . However, in IPF, dominated, whereas the percentage of reads assigned to in the same group was significantly lower than the percentage found in subjects with CHP. At the genus level, the burden was increased in CHP, and and burdens were increased in IPF. The lower airway bacterial burden in subjects with CHP was higher than that in control subjects but lower than that of those with IPF. In contrast to IPF, there was no association between bacterial burden and survival in CHP. The microbial profile of the lower airways in subjects with CHP is distinct from that of IPF, and, notably, the bacterial burden in individuals with CHP fails to predict survival.
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T.M.M. is Associate Editor of AJRCCM. His participation complies with American Thoracic Society requirements for recusal from review and decisions for authored works.
ISSN:1073-449X
1535-4970
1535-4970
DOI:10.1164/rccm.202002-0460OC