Iron Regulation and Biofilm Formation in Pseudomonas aeruginosa

Pseudomonas aeruginosa, an opportunistic Gram-negative pathogen, orchestrates a finely tuned network of iron acquisition and storage mechanisms that underpin its capacity to form resilient biofilms. Iron, though essential for critical cellular processes, is scarcely available in aerobic and host environments, prompting the bacterium to secrete high‐affinity siderophores such as pyoverdine and pyochelin. Uptake of ferric iron is governed by specific outer‐membrane receptors, while intracellular iron levels are sensed by the ferric uptake regulator (Fur), which represses or activates gene circuits in response to cytosolic iron. Excess iron is sequestered in bacterioferritin (BfrB), from which it can be mobilised by the BfrB–ferredoxin (Bfd) complex when demand exceeds supply. Concurrently, biofilm development—a multicellular lifestyle encapsulated within an extracellular polymeric substance—is closely linked to iron homeostasis. Iron deprivation generally stimulates biofilm maturation via second messenger signalling and altered expression of adhesins and exopolysaccharides, whereas iron abundance can enhance motility and dispersion. This dynamic interplay enables P. aeruginosa to adapt to fluctuating iron availability in diverse niches, from environmental reservoirs to chronic infections, and underlies its persistence in biofilm‐associated disease states such as cystic fibrosis and device‐related infections.

Research from Nature Portfolio

Investigation of airway mucus interactions has revealed a previously unrecognised siderophore system essential for P. aeruginosa survival in mucosal secretions. A novel genetic locus, independent of the canonical pyoverdine and pyochelin pathways, encodes proteins that facilitate iron scavenging from host-derived complexes. Disruption of this system leads to pronounced loss of viability in airway mucus, while genetic complementation with a phytosiderophore mimic restores intracellular iron levels and infectivity in vivo. This work highlights an adaptive iron‐uptake strategy that enables P. aeruginosa to exploit unique host iron reservoirs during early stages of airway colonisation.

Iron Regulation and Biofilm Formation in Pseudomonas aeruginosa publication trend

The graph below shows the total number of articles in iron regulation and biofilm formation in pseudomonas aeruginosa across all publications each year (not limited to Nature Index journals).

Technical terms

Siderophore: bacterial small molecule that binds ferric iron with high affinity to facilitate uptake under iron-limited conditions.

Biofilm: structured microbial community encased in an extracellular polymeric matrix attached to a biotic or abiotic surface.

Ferric uptake regulator (Fur): transcriptional repressor that senses cytosolic iron levels and modulates expression of iron-acquisition genes.

Bacterioferritin (BfrB): protein that stores ferric iron intracellularly, serving as a reservoir for future metabolic demands.

Ferredoxin (Bfd): iron–sulphur protein that binds to bacterioferritin to facilitate reduction and release of stored iron as Fe2+.

References

1. Pseudomonas aeruginosa senses and responds to epithelial potassium flux via Kdp operon to promote biofilm. PLOS Pathogens (2024).
2. A novel siderophore system is essential for the growth of Pseudomonas aeruginosa in airway mucus. Scientific Reports (2015).
3. Inhibiting Iron Mobilization from Bacterioferritin in Pseudomonas aeruginosa Impairs Biofilm Formation Irrespective of Environmental Iron Availability. ACS Infectious Diseases (2020).