Pulmonary Fibrosis Flare-up Changes Patients’ Respiratory Bacteria Mix, Study Reports

Pulmonary Fibrosis Flare-up Changes Patients’ Respiratory Bacteria Mix, Study Reports

When idiopathic pulmonary fibrosis (IPF) patients experience sharp flares and sudden disease worsening, the bacterial make-up of their respiratory tract changes, a study has found.

The research, “Changes in the respiratory microbiome during acute exacerbations of idiopathic pulmonary fibrosis,” compared patients whose condition had worsened because of an acute IPF exacerbation (AE-IPF) with those whose IPF had remained stable.  The findings were published in the journal Respiratory Research.

IPF patients can experience a significant respiratory deterioration unrelated to infection by common respiratory pathogens. Several pieces of evidence suggest the worsening may reflect previous exposure to bacteria or to unidentified “hidden” microorganisms in the respiratory microbiome, or microbe community.

Researchers collected lung fluid from 20 AE-IPF and 15 IPF patients through a procedure known as bronchoalveolar lavage (BAL).

They found that the cellular composition of BAL fluid was different between the two patient groups. There were more neutrophils, a type of inflammatory cell, in the lavage of AE-IPF patients.

By analyzing the bacterial DNA content in BALs, researchers identified different types of microorganisms in patients’ respiratory tracts. Bacterial communities of IPF patients contained Streptococcus, Prevotella, Veillonella, Haemophilus and Pseudomonas, which are also commonly found in the airways of healthy individuals.

In AE-IPF patients, there was an increase in two potentially pathogenic bacterial species,  Campylobacter and Stenotrophomonas. Campylobacter is a gastrointestinal pathogen sometimes found in the respiratory tract.

“Its presence in the respiratory microbiota is likely to arise from silent micro-aspiration of gastric contents and strengthens the already identified association of reflux and aspiration with acute exacerbations in a subgroup of patients,” the authors wrote.

The bacteria Stenotrophomonas is found in patients who have tubes in their airways that are connected to ventilators to help them breathe. The bacteria may cause infection in patients with chronic health conditions.

Results “suggest that bacteria may play a causative role in some AE-IPF. The apparent translocation of bacteria usually confined to the gastrointestinal tract also suggests a role for aspiration in the development of acute exacerbations,” the team concluded.

But researchers also noted the study had limitations. One was that collecting samples from AE-IPF patients is difficult and risky. Also, some patients received antibiotics before their samples were taken, which could have changed the type of microorganisms found.

To further test the hypothesis that microbiome alterations contribute to AE-IPF, samples should be collected before and during an exacerbation, the team said.

Despite these limitations, the authors suggested that because of the severity of AE-IPF, antimicrobial therapy should be considered early in an acute IPF exacerbation. “Nonetheless, our observations challenge the current paradigm for AE-IPF and provide a rationale for clinical trials of prophylactic antibiotics as a strategy to prevent acute exacerbations in individuals with IPF,” the team concluded.

 

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