Inhibiting Iron Mobilization from Bacterioferritin in Pseudomonas aeruginosa Impairs Biofilm Formation Irrespective of Environmental Iron Availability.
Anabel SoldanoHuili YaoJosephine R ChandlerMario RiveraPublished in: ACS infectious diseases (2020)
Although iron is essential for bacteria, the nutrient presents problems of toxicity and solubility. Bacteria circumvent these problems with the aid of iron storage proteins where Fe3+ is deposited and, when necessary, mobilized as Fe2+ for metabolic requirements. In Pseudomonas aeruginosa, Fe3+ is compartmentalized in bacterioferritin (BfrB), and its mobilization as Fe2+ requires specific binding of a ferredoxin (Bfd) to reduce the stored Fe3+. Blocking the BfrB-Bfd complex leads to irreversible iron accumulation in BfrB and cytosolic iron deprivation. Consequently, given the intracellular iron sufficiency requirement for biofilm development, we hypothesized that blocking the BfrB-Bfd interaction in P. aeruginosa would impair biofilm development. Our results show that planktonic and biofilm-embedded cells where the BfrB-Bfd complex is blocked exhibit cytosolic iron deficiency, and poorly developed biofilms, even in iron-sufficient culture conditions. These results underscore inhibition of the BfrB-Bfd complex as a rational target to dysregulate iron homeostasis and possibly control biofilms.
Keyphrases
- iron deficiency
- pseudomonas aeruginosa
- biofilm formation
- candida albicans
- staphylococcus aureus
- cystic fibrosis
- mental health
- escherichia coli
- oxidative stress
- signaling pathway
- risk assessment
- cell proliferation
- metal organic framework
- induced apoptosis
- ionic liquid
- human health
- room temperature
- reactive oxygen species
- transcription factor
- dna binding
- pi k akt
- innate immune