Rationale: Despite growing evidence for the roles of airway remodelling and bacterial infection in the progression of non-cystic fibrosis bronchiectasis, relationships between collagen degrading proteases and chronic airway infection are poorly understood. Objectives: This study aimed to determine which matrix metalloproteinases (MMPs) were elevated in bronchiectasis, whether these MMP levels varied based on patients' dominant infective microbe, and how these levels correlate with clinical measures of disease severity. Methods: We determined concentrations of nine MMPs and four tissue inhibitors of metalloproteinases (TIMPs) in induced sputum from 86 bronchiectasis patients and 8 healthy controls by Luminex protein assay. Concentrations were then assessed in relation to lung function, inflammatory markers and airway microbiota composition, determined by 16S rRNA gene amplicon sequencing. Airway microbiota composition was classified as Pseudomonas aeruginosa-dominated, Haemophilus influenzae-dominated or dominated by another species. MMP-8 and MMP-9 activity levels were also measured in a subset of patients. Measurements and Main Results: MMP-1, 3, 7, 8 and 9, and TIMP-2 and 4, as well as ratios of MMP-8/TIMP-1 and MMP-9/TIMP-1 were significantly higher in bronchiectasis patients than healthy controls (all p<0.001 except MMP-7 p<0.05). Bronchiectasis patients with H. influenzae-dominated airway infections demonstrated higher MMP-2 levels (p<0.01) and MMP-8 activity (p<0.05) than those with P. aeruginosa. Within bronchiectasis subjects, there were significant inverse correlations between FEV1 % and MMP-8, MMP-1 levels and MMP-8/TIMP-1 and MMP-9/TIMP-1 ratios (p<0.01). Conclusions: Increased MMP levels (particularly MMP-8 and MMP-1) and MMP/TIMP ratios in bronchiectasis patients compared to healthy controls correlated with lower lung function and higher levels of inflammatory markers. Further, MMP profiles differed in bronchiectasis patients according to the dominant pathogen determined by gene sequencing, raising the possibility of differential airway remodelling according to airway microbiology.