4.7 Article

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

Journal

Publisher

AMER THORACIC SOC
DOI: 10.1164/rccm.202002-0460OC

Keywords

lung microbiota; 16S; fibrosis

Funding

  1. Action for Pulmonary Fibrosis Mike Bray Fellowship
  2. National Institute for Health Research Clinician Scientist Fellowship [CS-2013-13-017]
  3. British Lung Foundation Chair in Respiratory Research grant [C17-3]
  4. Wellcome Senior Fellowship in Basic Biomedical Science [107059/Z/15/Z]
  5. Wellcome Trust [205949/Z/17/Z]
  6. Asthma UK senior fellowship [AUK-SNF-2017-381]
  7. Wellcome Trust [205949/Z/17/Z] Funding Source: Wellcome Trust

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The study found distinct differences in the lower airway microbial profiles of patients with Chronic Hypersensitivity Pneumonitis (CHP) and Idiopathic Pulmonary Fibrosis (IPF), with CHP patients' bacterial burden failing to predict survival.
Rationale: 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. Objectives: To characterize and compare the airway microbiome in subjects with CHP, subjects with idiopathic pulmonary fibrosis (IPF), and control subjects. Methods: We prospectively recruited individuals with a CHP diagnosis (n = 110), individuals with an IPF diagnosis (n = 45), and control subjects (n = 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. Measurements and Main Results: 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 Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. However, in IPF, Firmicutes dominated, whereas the percentage of reads assigned to Proteobacteria in the same group was significantly lower than the percentage found in subjects with CHP. At the genus level, the Staphylococcus burden was increased in CHP, and Actinomyces and Veillonella 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. Conclusions: 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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