Pseudomonas aeruginosa is a ubiquitous gram-negative bacterium and opportunistic human pathogen infecting immunocompromised individuals. P. aeruginosa causes acute infections in airways, bloodstream and surgery wounds and is the primary cause of mortality in patients affected with chronic pathologies, including chronic wounds, cystic fibrosis (CF) and cancer.
P. aeruginosa’s success as a pathogen is still not fully understood. One explanation may reside in its variegated genome composition and its adaptive plasticity. P. aeruginosa metabolism is exceptionally rich and branched, and the bacterium can rely on a broad set of virulence factors and stress resistance mechanisms. Population-level behaviours, such as biofilm formation, antibiotic resistance/persistence, virulence coordination through quorum sensing and the use of prophages as a defence mechanism enhances P. aeruginosa survival in the host. Moreover, the high mutational rate favours a quick physiological rewiring of the gene expression program, further supporting the adaptation to the host.
Overall, P.aeruginosa characteristics allow an environmental clone to successfully infect a host, often by directly hijacking and modulating host defences. Evolution through the acquisition of genetic mutations also relates to the rapid emergence of antibiotic resistance. For this reason, P. aeruginosa is one of the six ESKAPE pathogens identified by the WHO. Therefore, administration of effective treatments for both acute andchronic P. aeruginosa infections is becoming a challenging task.
Although antibiotic resistance is a severe threat, P. aeruginosa intrinsic antibiotic tolerance is additionally recognized as a critical step for the evolution of antibiotic resistance. Therefore, it should also be the focus of research and treatment development. To address P. aeruginosa infections, and the current and future issues it poses requires an in-depth knowledge of how the bacterium coordinates the systems that underlie its success as a pathogen and how it interacts with the host immune system.
This Research Topic aims to improve our understanding of the biology of P. aeruginosa infections and its interaction with the host to provide novel research data and ideas for building future P. aeruginosa treatments.
In particular, we seek Original Research articles and up-to-date Reviews that cover, but are not limited to, the following topics:
1. The role of metabolic and regulatory networks in P. aeruginosa pathogenesis, including virulence factor production, biofilm formation, antibiotic tolerance, and resistance.
2. Mechanisms supporting P.aeruginosa survival in the host and/or in the environment, including acquisition of restricted nutrients, stress response, drug tolerance and resistance.
3. The role of host innate and adapted immunity in response to P. aeruginosa infections and pathogen immune evasion.
4. Novel factors underlining the interactions between P. aeruginosa and the host.
5. New therapeutic approaches targeting both P. aeruginosa persistence mechanisms and the host response.
Pseudomonas aeruginosa is a ubiquitous gram-negative bacterium and opportunistic human pathogen infecting immunocompromised individuals. P. aeruginosa causes acute infections in airways, bloodstream and surgery wounds and is the primary cause of mortality in patients affected with chronic pathologies, including chronic wounds, cystic fibrosis (CF) and cancer.
P. aeruginosa’s success as a pathogen is still not fully understood. One explanation may reside in its variegated genome composition and its adaptive plasticity. P. aeruginosa metabolism is exceptionally rich and branched, and the bacterium can rely on a broad set of virulence factors and stress resistance mechanisms. Population-level behaviours, such as biofilm formation, antibiotic resistance/persistence, virulence coordination through quorum sensing and the use of prophages as a defence mechanism enhances P. aeruginosa survival in the host. Moreover, the high mutational rate favours a quick physiological rewiring of the gene expression program, further supporting the adaptation to the host.
Overall, P.aeruginosa characteristics allow an environmental clone to successfully infect a host, often by directly hijacking and modulating host defences. Evolution through the acquisition of genetic mutations also relates to the rapid emergence of antibiotic resistance. For this reason, P. aeruginosa is one of the six ESKAPE pathogens identified by the WHO. Therefore, administration of effective treatments for both acute andchronic P. aeruginosa infections is becoming a challenging task.
Although antibiotic resistance is a severe threat, P. aeruginosa intrinsic antibiotic tolerance is additionally recognized as a critical step for the evolution of antibiotic resistance. Therefore, it should also be the focus of research and treatment development. To address P. aeruginosa infections, and the current and future issues it poses requires an in-depth knowledge of how the bacterium coordinates the systems that underlie its success as a pathogen and how it interacts with the host immune system.
This Research Topic aims to improve our understanding of the biology of P. aeruginosa infections and its interaction with the host to provide novel research data and ideas for building future P. aeruginosa treatments.
In particular, we seek Original Research articles and up-to-date Reviews that cover, but are not limited to, the following topics:
1. The role of metabolic and regulatory networks in P. aeruginosa pathogenesis, including virulence factor production, biofilm formation, antibiotic tolerance, and resistance.
2. Mechanisms supporting P.aeruginosa survival in the host and/or in the environment, including acquisition of restricted nutrients, stress response, drug tolerance and resistance.
3. The role of host innate and adapted immunity in response to P. aeruginosa infections and pathogen immune evasion.
4. Novel factors underlining the interactions between P. aeruginosa and the host.
5. New therapeutic approaches targeting both P. aeruginosa persistence mechanisms and the host response.