# Clinical implications of traction bronchiectasis in IPF and fibrotic RA-ILD – a retrospective single-center cohort study

**Authors:** Jakob Raith, Jannik Ruwisch, Jonas C Schupp, Theresa Graalmann, Nora Drick, Marius M Hoeper, Antje Prasse, Jan Fuge, Felix C Ringshausen, Leonard Knegendorf, Jessica Rademacher, Sabine Dettmer, Benjamin Seeliger

PMC · DOI: 10.1186/s12931-026-03497-6 · Respiratory Research · 2026-01-13

## TL;DR

Traction bronchiectasis in IPF and RA-ILD is linked to fibrosis severity and higher mortality, but not to typical bronchiectasis symptoms.

## Contribution

This study identifies traction bronchiectasis as a marker of fibrotic remodeling rather than a distinct syndrome in ILD.

## Key findings

- Higher bronchiectasis scores correlated with fibrosis extent and lower baseline lung function.
- Increased bronchiectasis scores were independently associated with higher mortality in IPF and RA-ILD patients.
- Pathogen detection was common but not linked to bronchiectasis severity or clinical outcomes.

## Abstract

Bronchiectasis is a common feature in idiopathic pulmonary fibrosis (IPF) and rheumatoid arthritis-associated interstitial lung disease (RA-ILD). While these so-called traction bronchiectasis are often considered a secondary phenomenon in fibrosing ILD, their prognostic significance and relationship to respiratory pathogen detection and outcomes remain unclear.

We conducted a retrospective, single-center cohort study in IPF or fibrosing RA-ILD patients with available high-resolution computed tomography (HRCT) and lower-respiratory tract microbial samples between 2014 and 2024. Bronchiectasis was assessed using the bronchiectasis subscore of the Brody score; fibrosis was quantified by deep-learning–based automated HRCT analysis. Primary outcome was 5-year transplant-free survival; secondary outcomes included isolation of pathogens per CDC criteria, PFT trajectories, bronchiectasis-associated symptoms, and hospitalization. Statistical methods included Cox regression, linear mixed-effects modeling and correlation analysis.

267 IPF and 56 RA-ILD patients were included. Median modified Brody score was 11.5 (IQR 7–16; max possible range 0–72). Higher Brody scores strongly correlated with fibrotic extent (R = 0.6, P < 0.001). Higher scores had significantly lower baseline FVC and DLCO (P < 0.001), but no differences in PFT trajectories over time. In multivariable Cox regression, higher bronchiectasis scores were independently associated with mortality (HR 1.03 per point [95%CI 1.01–1.06], P = 0.003); fibrosis extent showed similar results (HR 1.02, CI 1.00–1.03, P = 0.017). Pathogens were found at a median of 3 months after baseline in 50.9% (IPF) and 46.4% (RA-ILD), without association with survival, symptoms or Brody scores. Staphylococcus aureus was most common (28.9%); Pseudomonas aeruginosa was rare (1.9%).

In both IPF and RA-ILD, higher bronchiectasis scores were associated with fibrosis extent and mortality, but not classical clinical bronchiectasis features. This supports traction bronchiectasis as a marker of fibrotic remodeling rather than a distinct syndrome.

Not applicable.

The online version contains supplementary material available at 10.1186/s12931-026-03497-6.

## Linked entities

- **Diseases:** idiopathic pulmonary fibrosis (MONDO:0800029), rheumatoid arthritis-associated interstitial lung disease (MONDO:0004586), bronchiectasis (MONDO:0004822)

## Full-text entities

- **Genes:** MUC5B (mucin 5B, oligomeric mucus/gel-forming) [NCBI Gene 727897] {aka MG1, MUC-5B, MUC5, MUC9}, CTD (Coats disease) [NCBI Gene 1283]
- **Diseases:** emphysema (MESH:D004646), neutrophilic (MESH:C564275), CF (MESH:D003550), chronic cough (MESH:D003371), alveolar injury (MESH:D014947), GERD (MESH:D005764), death (MESH:D003643), Sjoegren's Disease (MESH:D004194), primary ciliary dyskinesia (MESH:D002925), weight loss (MESH:D015431), COPD (MESH:D029424), Bronchiectasis (MESH:D001987), fungal (MESH:D009181), bronchial disease (MESH:D001982), follicular bronchiolitis (MESH:D001988), fibrotic lung (MESH:D008171), post COVID-19 (MESH:D000094024), associated (MESH:D018886), systemic diseases (MESH:D034721), Connective Tissue Disease (MESH:D003240), Neutrophilic inflammation (MESH:D007249), pneumonia (MESH:D011014), ERS (MESH:C000719191), chronic infection (MESH:D000088562), IPF (MESH:D054990), infection (MESH:D007239), Interstitial Pneumonia (MESH:D017563), PPF (MESH:D011658), bacterial infection (MESH:D001424), RA (MESH:D001172), heartburn (MESH:D006356), respiratory (MESH:D012131), fibrosing (MESH:D005355), neutrophilia (MESH:C563010)
- **Chemicals:** Oxygen (MESH:D010100), hypertonic saline (MESH:D012965), Carbon Monoxide (MESH:D002248), cyclic citrullinated (-)
- **Species:** Haemophilus parainfluenzae (species) [taxon 729], Homo sapiens (human, species) [taxon 9606], Pseudomonas aeruginosa (species) [taxon 287], Mycobacterium tuberculosis (species) [taxon 1773], Haemophilus influenzae (species) [taxon 727], Enterobacteriaceae (enterobacteria, family) [taxon 543], Staphylococcus aureus (species) [taxon 1280]

## Full text

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## Figures

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## References

13 references — full list in the complete paper: https://tomesphere.com/paper/PMC12849085/full.md

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Source: https://tomesphere.com/paper/PMC12849085