Abstract

Background Acute exacerbation of IPF (AE-IPF) is associated with high mortality. We studied changes in pathogen involvement during AE-IPF and explored a possible role of infection in AE-IPF. Objectives Our purpose is to investigate the role of infection in AE-IPF. Methods Overall, we recruited 170 IPF patients (48 AE-IPF, 122 stable) and 70 controls at Shanghai Pulmonary Hospital. Specific IgM against microbial pathogens and pathogens in sputum were assessed. RNA sequences of pathogens in nasopharyngeal swab of IPF patients were detected by PathChip. A panel of serum parameters reflecting immune function were assessed. Results Antiviral/bacterial IgM was higher in IPF vs. controls and in AE-IPF vs. stable IPF. Thirty-eight different bacterial strains were detected in IPF patient sputum. Bacteria-positive results were found in 9/48 (18.8%) of AE-IPF and in 26/122 (21.3%) stable IPF. Fifty-seven different viruses were detected in nasopharyngeal swabs of IPF patients. Virus-positive nasopharyngeal swabs were found in 18/30 (60%) of tested AE-IPF and in 13/30 (43.3%) of stable IPF. AE-IPF showed increased inflammatory cytokines (IL-6, IFN-γ, MIG, IL-17, and IL-9) vs. stable IPF and controls. Mortality of AE-IPF in one year (39.5%) was higher compared to stable IPF (28.7%).Conclusions. IPF patients had different colonization with pathogens in sputum and nasopharyngeal swabs; they also displayed abnormally activated immune response, which was exacerbated during AE-IPF.

Highlights

  • Acute exacerbation of Idiopathic pulmonary fibrosis (IPF) (AE-IPF) is associated with high mortality

  • An international working group had suggested that it would be important to rule out obvious infections for IPF patients with deteriorating symptoms over less than one month but had acknowledged that AE following a triggering event might end as bad as idiopathic AE episodes [10]

  • We aimed to investigate the association of Acute exacerbation of IPF (AE-IPF) with microbial colonization and/or latent infection

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Summary

Introduction

Acute exacerbation of IPF (AE-IPF) is associated with high mortality. We studied changes in pathogen involvement during AE-IPF and explored a possible role of infection in AE-IPF. RNA sequences of pathogens in nasopharyngeal swab of IPF patients were detected by PathChip. Thirty-eight different bacterial strains were detected in IPF patient sputum. Fifty-seven different viruses were detected in nasopharyngeal swabs of IPF patients. IPF patients had different colonization with pathogens in sputum and nasopharyngeal swabs; they displayed abnormally activated immune response, which was exacerbated during AE-IPF. Patients with IPF have a median survival time of 3 years [1], following either a progressive course of worsening respiratory function, or a more rapid decline described as acute exacerbation (AE-IPF) [2]. The common criteria for AE-IPF include a diagnosis of IPF with acute worsening of dyspnea in the preceding month, new radiographic opacities or ground glass on computed tomography (CT), and exclusion of alternative causes (e.g., infection, congestive heart failure, and pulmonary embolism). The fundamental to the concept of idiopathic AE-IPF is Mediators of Inflammation

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