Microbiota and fungal-bacterial interactions in the Cystic Fibrosis lung.

The most common genetic hereditary disease affecting Caucasians is Cystic Fibrosis (CF), which is caused by autosomal recessive mutations in the CFTR gene. The most serious consequence is the production of a thick and sticky mucus in the respiratory tract, which entraps airborne microorganisms and facilitates colonization, inflammation, and infection. Therefore, the present article compiles the information about the microbiota and, particularly, the inter-kingdom fungal-bacterial interactions in the CF lung, the molecules involved, and the potential effects that these interactions may have on the course of the disease. Among the bacterial compounds, quorum sensing-regulated molecules such as homoserine lactones, phenazines, rhamnolipids, quinolones, and siderophores (pyoverdine and pyochelin) stand out, but volatile organic compounds, maltophilin, and CF-related bacteriophages are also explained. These molecules exhibit diverse antifungal mechanisms, including iron starvation and induction of reactive oxygen and nitrogen species production. The fungal compounds are less studied, but they include cell wall components, siderophores, patulin, and farnesol. Despite the apparent competition between microorganisms, the persistence of significant rates of bacterial-fungal co-colonization in CF suggests that numerous variables influence it. In conclusion, it is crucial to increase scientific and economic efforts to intensify studies on the bacterial-fungal inter-kingdom interactions in the CF lung.