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The bronchiectasis biobank and airway microbiome

Decades of banked airway samples, read with modern sequencing and immune profiling, to understand what makes an exacerbation happen.

Background

Exacerbations are what make bronchiectasis progressive. They drive lung function decline, hospitalisation, and repeated antibiotic exposure — and they are still managed reactively, once damage has already occurred. Treatment decisions rest largely on culture results, empiric antibiotic choices, and anti-inflammatory therapies given without biological stratification, so patients with very different airway biology are often managed in much the same way.

The difficulty is not detecting microbes. It is that a pathogen name does not predict a trajectory. Two people can culture the same organism and follow entirely different courses: one improves on treatment that on paper should not have worked, while another stays inflamed through escalation. What is missing is a way of reading the airway as an ecosystem and as an immune environment at the same time.

What we are doing

The University of Calgary maintains one of the largest longitudinal bronchiectasis sputum and bacterial biobanks anywhere, built over four decades and linked to detailed clinical data. Its defining feature is repeated within-person sampling across clinical stability, exacerbation, and recovery — which lets us watch airway states change over time rather than infer them from a single snapshot.

Across this collection we are building an integrated picture of the airway:

  • Long-read metagenomic sequencing, resolving bacteria, fungi, viruses, antimicrobial resistance genes, and functional gene content in a single assay;
  • High-dimensional immune profiling of the airway, paired with soluble inflammatory mediators and measures of neutrophil activity;
  • Integration of the two, to derive a small, interpretable set of airway endotypes — reproducible host–microbe configurations linked to distinct clinical trajectories.

Alongside the microbial work, we are asking how the immune response behaves after an exacerbation resolves. One of our central questions is whether clinical recovery is the same thing as biological recovery, or whether some patients carry inflammation forward into the interval that is meant to be well — which would help explain why exacerbations cluster in the same individuals.

Why it matters

If airway endotypes prove reproducible and anchored to outcomes, they become actionable risk states: a way of identifying who is deteriorating before the deterioration is visible, and a rational basis for choosing between antimicrobial and host-directed treatment. Asthma made this transition when inflammatory endotyping enabled targeted biologics. Bronchiectasis has not yet, and broad, unstratified treatment is part of the reason therapies help some patients and not others. Our aim is to build the biological foundation that stratified prevention trials will need.