# Evidence and role for bacterial mucin degradation in cystic fibrosis airway disease

## TL;DR

Bacterial breakdown of mucins in the lungs of cystic fibrosis patients may provide nutrients that support harmful pathogens.

## Contribution

The study reveals that oral anaerobes ferment mucins to produce nutrients that sustain pathogens in the CF lung.

## Key findings

- Oral anaerobes can grow on mucins and produce propionate and acetate.
- Propionate is linked to increased P. aeruginosa gene activity in CF sputum.
- Mucin fermentation by commensal bacteria may fuel pathogen growth in the airways.

## Abstract

Chronic respiratory infections are composed of complex microbial communities that incite persistent inflammation and airway damage. Despite the high density of bacteria that colonize the airways, nutrient sources that sustain bacterial growth in vivo are unknown. Here we examine the role of respiratory mucins in the ecological dynamics of the cystic fibrosis lung microbiota. While P. aeruginosa was unable to efficiently utilize mucins, saliva-derived anaerobes stimulated the growth of opportunistic pathogens when provided mucins as the sole carbon source. The fermentative metabolisms of these oral anaerobes generated amino acids and short chain fatty acids (propionate and acetate) during mucin enrichment in vitro, which were also found within expectorated sputum from CF patients. The significance of these findings was supported by in vivo P. aeruginosa gene expression, which revealed a heightened response to propionate. Given that propionate is exclusively derived from bacterial fermentation, these data support a central role for mucin fermentation in the carbon flux of the lower airways. More specifically, commensal oral bacteria may contribute to airway disease by degrading mucins, in turn providing nutrients for pathogens otherwise unable to obtain carbon in the lung.