Abstract

Common complications associated with diabetes are chronic wounds and lung infections caused by biofilms, surface-associated bacterial communities encased in a polymeric matrix. However, it is unclear why diabetes enhances the prevalence of biofilms. Recent findings indicated insulin, a key player in diabetes, to enhance biofilm formation. As biofilms are associated with high c-di-GMP levels, and phosphodiesterases (PDEs) degrade intracellular signal c-di-GMP, we asked if insulin enhances Pseudomonas aeruginosa biofilm formation by inhibiting PDE activity. 

PDE enzyme assays carried out in the presence and absence of insulin indicated insulin to significantly suppress PDE activity. To identify which PDEs are responsive to insulin, we screened 24 PDE mutant strains. Interestingly, the majority of PDE mutant strains were non-responsive to insulin, suggesting insulin to have a global effect on PDE activity and thus, c-di-GMP levels. Future work will explore PDE activators as a therapeutic to combat biofilm infections in diabetic patients.