Iron chelation as novel treatment for lung inflammation in cystic fibrosis.

Cystic fibrosis (CF) is an autosomal recessive genetic disorder that results in defective cystic fibrosis transmembrane conductance regulator (CFTR) protein expression and function in various tissues. The leading cause of CF mortality and morbidity is the progressive destruction of the lungs due to recurrent infections and chronic inflammation. CFTR defect also affects immune cells, including neutrophils, resulting in ineffective, severe and persistent inflammatory response. Since unopposed recruitment of neutrophils significantly contributes to lung tissue damage through the generation of reactive oxygen species (ROS), we hypothesize that the administration of iron chelators could serve as a novel treatment to attenuate chronic inflammation in CF lungs since iron is significantly involved in ROS production by neutrophils. Ideally, the iron chelator should sequester host iron effectively, prevent bacterial access to chelator-bound iron and penetrates lung tissues efficiently, e.g. by inhalational route of administration.

Robust synthesis of F-BODIPYs.

A protocol is established for the high-yielding synthesis of F-BODIPYs involving non-anhydrous reagents and not requiring precautions to exclude moisture. This simple and robust strategy simply requires a second addition of NEt3 and BF3·OEt2, midway through the reaction period. The ratio and amounts of NEt3 and BF3·OEt2 used in each aliquot are critical to success (6 : 9 for each aliquot). The protocol can be completed using bench-dry apparatus, without need to achieve and maintain anhydrous conditions or solvents.