Multi-omics technologies characterize neutrophil-microbe interactions in bronchiectasis sputum

Bronchiectasis is a chronic lung disease marked by airway dilation, persistent cough, sputum production and recurrent infections. The pathophysiology involves genetic predispositions, dysregulated inflammation and host-pathogen interactions. Neutrophils are key drivers of disease progression, contributing to tissue damage and lung function decline through their secretions and antimicrobial activity. To investigate how microbial shifts influence host responses, we analyzed induced sputum from 31 stable bronchiectasis patients across a range of disease severity. ELISA quantification of neutrophil-recruiting chemokines, such as CXCL1 and CXCL8 correlated with clinical severity and an increase in neutrophil subset counts, as identified by multi-color flow cytometry. Single-cell RNA sequencing revealed 4 distinct neutrophil transcriptional states in severe cases, marked by genes involved in extracellular matrix degradation, TLR signaling, cytokine responses, degranulation and phagocytosis. Complementary 16S rRNA sequencing showed reduced microbial richness which correlated with diminished lung function and disease severity. We identified 21 taxa significantly associated with disease severity and uncovered links between commensal microbe composition and neutrophil expression of genes related to cytokine signaling, cell adhesion, lysosome acidification, as well as proteases. Together, these findings highlight the dynamic interplay between neutrophil activity and microbial dysbiosis in bronchiectasis pathogenesis. Publication History Article published online: 04 March 2026 © 2026. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany