The structure–function relationship ofPseudomonas aeruginosain infections and its influence on the microenvironment

Abstract

Pseudomonas aeruginosa is a human pathogen associated with both acute and chronic infections. While intensively studied, the basic mechanisms enabling the long-term survival of P. aeruginosa in the host, despite massive immune system attack and heavy antimicrobial treatment, remain to be identified. We argue that such infections may represent niche invasions by P. aeruginosa that influence the microenvironment by depleting host-derived substrate and activating the immune response. Bacteria embedded in cell aggregates establish a microenvironmental niche, where they endure the initial host response by slowing down their metabolism. This provides stable, lasting growth conditions with a constant, albeit slow supply of substrate and electron acceptors. Under such stable conditions, P. aeruginosa exhibits distinct adaptive traits, where its gene expression pattern reflects a life exposed to continuous attack by the host immune system and antimicrobials. Here we review fundamental microenvironmental aspects of chronic P. aeruginosa infections and examine how their structural organization influences their in vivo microenvironment, which in turn affects the interaction of P. aeruginosa biofilm aggregates with the host immune system. We discuss how improving our knowledge about the microenvironmental ecology of P. aeruginosa in chronic infections can be used to combat persistent, hard-to-treat bacterial infections.

Investigation of the Mechanism and Chemistry Underlying Staphylococcus aureus ' Ability to Inhibit Pseudomonas aeruginosa Growth In Vitro

“… P. aeruginosa colonizes later and is prevented from mixing and overgrowing S. aureus . P. aeruginosa establishes populations within a distance to S. aureus (calling-distance,10 to 50 μm, refer to reference ( 68 )), and P. aeruginosa also produces S. aureus -inhibiting substances keeping the two species apart. Thereby, the coexistence of the two species is seen as separated single-species aggregates in coinfections, with synergy as a result, e.g., as increased virulence and antibiotic tolerance.…”

Treatment of Pseudomonas aeruginosa infectious biofilms: Challenges and strategies

“…When combined with tobramycin or ciprofloxacin, re-oxygenation with HBOT enhanced the killing of clinical P. aeruginosa and the eradication of biofilms (Lichtenberg et al, 2022).…”

Effect of Phthalates and Their Substitutes on the Physiology of Pseudomonas aeruginosa

“…Many of these virulence factors are tightly regulated by the three interconnected quorumsensing (QS) communication systems, two of which (the Las and Rhl systems) are based on the production and sensing of N-acyl-homoserine lactones (AHL), and the PQS system, which depends on 4-hydroxy-2-alkylquinolines (HAQ) [7]. Chronic infections are mostly associated with biofilms, which are organized communities of microorganisms bound to a surface or interface and/or to each other and are embedded into a self-produced exopolymeric matrix consisting of exopolysaccharides, extracellular DNA, outer membrane vesicles, and proteins [8,9], in association with secretions from infected tissue [10]. P. aeruginosa, similar to most bacteria, is able to form biofilms at the air/liquid interface known as pellicles [11].…”