Host-Pathogen Interactions in Pseudomonas Aeruginosa Infections

Pseudomonas aeruginosa is an opportunistic Gram-negative bacterium responsible for a spectrum of acute and chronic infections, notably in cystic fibrosis, burn wounds and ventilator-associated pneumonia. Its success as a pathogen lies in a multifaceted interplay with the host immune system: it deploys an array of virulence factors—such as secreted toxins, adhesins and proteases—while modulating host defences through biofilm formation, quorum sensing and intracellular survival. Initial colonisation often triggers a vigorous innate immune response, driven by neutrophils and macrophages, which in turn is subverted by bacterial evasion strategies including extracellular polymeric substance production and manipulation of phagocyte pathways. In chronic settings, P. aeruginosa adapts via mucoid phenotypes, small-colony variants and metabolic reprogramming, establishing persistent reservoirs that resist antibiotics and host clearance. Understanding these host–pathogen dynamics is vital for the development of innovative therapies that can disrupt biofilms, restore phagocytic function and rebalance host resistance and tolerance mechanisms.

Research from Nature Portfolio

Recent studies have elucidated the importance of intracellular stages in host phagocytes. One investigation using zebrafish and murine models showed that mutants lacking the outer membrane protein OprF are rapidly eliminated by macrophages, whereas wild-type bacteria persist in vacuoles or the cytoplasm, highlighting OprF as critical for intramacrophage survival and both acute and persistent infection. Another study examined the IL-17A axis in chronic airway colonisation, revealing that sustained IL-17A signalling enhances resistance to initial infection yet impairs tissue tolerance, leading to increased inflammation and remodelling. Blockade of IL-17A in established chronic infection improved host tolerance without compromising bacterial control, pointing to cytokine modulation as a promising strategy to mitigate tissue damage during long-term colonisation.

Host-Pathogen Interactions in Pseudomonas Aeruginosa Infections publication trend

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

Technical terms

Biofilm: A structured community of bacterial cells embedded in an extracellular matrix, conferring resistance to antibiotics and immune clearance.

Quorum sensing: Cell-to-cell communication via small signalling molecules that coordinate gene expression, including virulence factor production.

Innate immunity: The host’s first line of defence, comprising phagocytic cells (neutrophils, macrophages), antimicrobial peptides and inflammatory mediators.

Intramacrophage survival: The ability of bacteria to persist within macrophages, evading degradation in phagolysosomes or escaping into the cytosol.

Host tolerance: Mechanisms by which the host limits tissue damage during infection without necessarily reducing pathogen burden.

References

1. Intracellular Pseudomonas aeruginosa persist and evade antibiotic treatment in a wound infection model. PLOS Pathogens (2025).
2. Evaluating the In Vivo Virulence of Environmental Pseudomonas aeruginosa Using Microinjection Model of Zebrafish (Danio rerio). Antibiotics (2023).
3. Contribution of intramacrophage stages to Pseudomonas aeruginosa infection outcome in zebrafish embryos: insights from mgtC and oprF mutants. Scientific Reports (2024).
4. IL-17A impairs host tolerance during airway chronic infection by Pseudomonas aeruginosa. Scientific Reports (2016).