Coinfection with and in cystic fibrosis.

OBJECTIVES

Cystic fibrosis (CF) lung disease is characterised by mucus stasis, chronic infection and inflammation, causing progressive structural lung disease and eventual respiratory failure. CF airways are inhabited by an ecologically diverse polymicrobial environment with vast potential for interspecies interactions, which may be a contributing factor to disease progression. and are the most common bacterial and fungal species present in CF airways respectively and coinfection results in a worse disease phenotype.

METHODS

In this review we examine existing expert knowledge of chronic co-infection with and in CF patients. We summarise the mechanisms of interaction and evaluate the clinical and inflammatory impacts of this co-infection.

RESULTS

inhibits through multiple mechanisms: phenazine secretion, iron competition, quorum sensing and through diffusible small molecules. reciprocates inhibition through gliotoxin release and phenotypic adaptations enabling evasion of inhibition. Volatile organic compounds secreted by stimulate growth, while stimulates production of cytotoxic elastase.

CONCLUSION

A complex bi-directional relationship exists between and , exhibiting both mutually antagonistic and cooperative facets. Cross-sectional data indicate a worsened disease state in coinfected patients; however, robust longitudinal studies are required to derive causality and to determine whether interspecies interaction contributes to disease progression.