Pseudomonas Aeruginosa Pathogenicity in Cystic Fibrosis

Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen that establishes chronic lung infections in individuals with cystic fibrosis (CF). Following initial colonisation, the bacterium adapts through genetic and phenotypic changes, most notably conversion to a mucoid phenotype driven by overproduction of the exopolysaccharide alginate. This transition fosters the formation of biofilms—surface-attached communities embedded in an extracellular matrix—that confer resistance to host immunity and antibiotics. Within the CF airway, biofilms impede mucociliary clearance and limit penetration of therapeutic agents. Concurrently, P. aeruginosa deploys an array of virulence factors and regulatory networks, including two-component systems and cyclic di-GMP signalling, to modulate motility, toxin production and nutrient acquisition under oxidative stress. Adaptations such as alginate acetylation further enhance immune evasion by reducing opsonic phagocytosis and reactive oxygen species damage. The resulting persistent infection drives progressive airway inflammation and tissue damage. Understanding these interconnected processes—biofilm architecture, exopolysaccharide modification, inter-variant cooperation and regulatory regulation—remains central to developing novel antimicrobials and approaches to disrupt chronic colonisation in CF patients.

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Pseudomonas Aeruginosa Pathogenicity in Cystic Fibrosis publication trend

The graph below shows the total number of articles in pseudomonas aeruginosa pathogenicity in cystic fibrosis across all publications each year (not limited to Nature Index journals).

Technical terms

Mucoid phenotype: Overproduction of alginate by P. aeruginosa leading to a mucous-like biofilm in CF airways.

Alginate: An anionic exopolysaccharide polymer secreted by P. aeruginosa, forming the structural scaffold of biofilms.

Biofilm: A surface-attached microbial community embedded in an extracellular matrix that protects bacteria from host defences and antibiotics.

Exopolysaccharide: High-molecular-weight carbohydrate polymers secreted by bacteria contributing to biofilm matrix architecture.

Opsonisation: The process by which pathogens are labelled by host proteins, such as antibodies or complement, to promote phagocytosis.

Alginate acetylation: Enzymatic addition of acetyl groups to alginate, enhancing its capacity to resist immune clearance and maintain biofilm stability.

References

1. Mechanism of resistance to phagocytosis and pulmonary persistence in mucoid Pseudomonas aeruginosa. Frontiers in Cellular and Infection Microbiology (2023).
2. Mixed Communities of Mucoid and Nonmucoid Pseudomonas aeruginosa Exhibit Enhanced Resistance to Host Antimicrobials. mBio (2018).
3. Pseudomonas aeruginosa AlgF is a protein–protein interaction mediator required for acetylation of the alginate exopolysaccharide. Journal of Biological Chemistry (2023).
4. Pseudomonas aeruginosa Nonphosphorylated AlgR Induces Ribonucleotide Reductase Expression under Oxidative Stress Infectious Conditions. mSystems (2023).
5. ChIP-seq reveals the global regulator AlgR mediating cyclic di-GMP synthesis in Pseudomonas aeruginosa. Nucleic Acids Research (2015).
6. The Pseudomonas aeruginosa AlgZR two-component system coordinates multiple phenotypes. Frontiers in Cellular and Infection Microbiology (2014).