Pseudomonas Aeruginosa Pathogenesis in Corneal Infections

Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen responsible for aggressive corneal infections that can rapidly progress to vision-threatening keratitis. The pathogenesis involves initial adhesion to the damaged corneal epithelium, often facilitated by pili-mediated twitching motility and biofilm formation on the ocular surface or contact lenses. Following adhesion, bacteria deploy a suite of virulence factors, including the type III secretion system, elastases and proteases, to invade and degrade stromal tissue. Host responses are characterised by rapid neutrophil recruitment and cytokine release, which, while essential for bacterial clearance, also contribute to corneal opacity and scarring. In addition to cell-to-cell spread, P. aeruginosa exploits the precise architecture of the corneal stroma, using aligned collagen lamellae as conduits for deeper penetration. Recent advances have shed light on interkingdom communication via extracellular vesicles released by infected epithelial cells, which act as homing beacons for neutrophils. Together, these insights have informed new therapeutic strategies aimed at disrupting bacterial adhesion, blocking key virulence mechanisms and modulating the host inflammatory response to preserve corneal integrity and prevent vision loss.

Research from Nature Portfolio

Advanced imaging studies have used second harmonic generation and multiphoton fluorescence to visualise P. aeruginosa behaviour within the corneal stroma. These investigations revealed that the bacteria align closely with collagen lamellae, exploiting the uniform spacing of stromal fibres to facilitate lateral spread. Ex vivo and in vivo models demonstrated that this alignment enables rapid infiltration without crossing the limbus, highlighting the central cornea as a unique ecological niche. Such high-resolution mapping of bacterial trajectories has established collagen orientation as a determinant of infection dynamics and may guide the design of structural barriers or collagen-targeted therapies to impede stromal invasion.

Pseudomonas Aeruginosa Pathogenesis in Corneal Infections publication trend

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

Technical terms

Type III secretion system: A specialised protein-delivery apparatus that injects bacterial effectors into host cells to subvert immune defences and promote tissue invasion.

Biofilm: A structured community of bacteria encased in an extracellular polymeric matrix that adheres to surfaces and exhibits increased resistance to antimicrobial agents.

Twitching motility: Surface translocation driven by the extension and retraction of type IV pili, crucial for initial colonisation and microcolony formation.

Extracellular vesicles (EVs): Nano-sized membrane vesicles released by eukaryotic cells that carry proteins and nucleic acids, influencing intercellular communication and immune cell recruitment.

References

1. Extracellular vesicles released by host epithelial cells during Pseudomonas aeruginosa infection function as homing beacons for neutrophils. Cell Communication and Signaling (2024).
2. Corneal Infection Models: Tools to Investigate the Role of Biofilms in Bacterial Keratitis. Cells (2020).
3. Second harmonic generation imaging of corneal stroma after infection by Pseudomonas aeruginosa. Scientific Reports (2017).
4. Microbial Adherence to Contact Lenses and Pseudomonas aeruginosa as a Model Organism for Microbial Keratitis. Pathogens (2022).