Pseudomonas aeruginosa Biofilms

Abstract

Pseudomonas aeruginosa is an opportunistic human pathogen causing devastating acute and chronic infections in individuals with compromised immune systems. Its highly notorious persistence in clinical settings is attributed to its ability to form antibiotic-resistant biofilms. Biofilm is an architecture built mostly by autogenic extracellular polymeric substances which function as a scaffold to encase the bacteria together on surfaces, and to protect them from environmental stresses, impedes phagocytosis and thereby conferring the capacity for colonization and long-term persistence. Here we review the current knowledge on P. aeruginosa biofilms, its development stages, and molecular mechanisms of invasion and persistence conferred by biofilms. Explosive cell lysis within bacterial biofilm to produce essential communal materials, and interspecies biofilms of P. aeruginosa and commensal Streptococcus which impedes P. aeruginosa virulence and possibly improves disease conditions will also be discussed. Recent research on diagnostics of P. aeruginosa infections will be investigated. Finally, therapeutic strategies for the treatment of P. aeruginosa biofilms along with their advantages and limitations will be compiled.

Keywords: Pseudomonas aeruginosa; biofilms; quorum sensing.

Figure 1

Cycle of P. aeruginosa biofilm development. The development cycle is divided into six stages. Initially, the bacteria associate with the surface and produce extracellular polymeric substances (EPS) including proteins, polysaccharides, lipids and eDNA. Next, cell division and the transition of reversible attachment into irreversible take place. The following steps are the formation of microcolonies and the further development of these microcolonies into mushroom-shaped structures. Cell-to-cell interaction and production of virulence factors play essential roles in maturation and robustness of biofilms. Matrix cavity is then formed in the centre of microcolony via cell autolysis to disrupt the matrix for the liberation of the dispersed population. Finally, the released cells undergo an approximately 2 h transition into planktonic phenotypes which subsequently occupy uncolonized spaces.

Figure 2

Hierarchical quorum-sensing (QS) network in Pseudomonas aeruginosa. The four QS pathways are activated in response to the cell density and environmental stimuli, with four autoinducer synthases including LasI, RhlI, PqsABCDH and AmbBCDE that produce N-3-oxo-dodecanoyl-ʟ-homoserine lactone (3O-C₁₂-HSL), N-butyryl-ʟ-homoserine lactone (C₄-HSL), 2-heptyl-3-hydroxy-4-quinolone (PQS) and 2-(2-hydroxyphenyl)-thiazole-4-carbaldehyde (IQS), respectively. Note: the autoinduction is depicted in red arrows; the receptor for IQS is still unknown. The QS products are secreted through the cell membrane, that control the group behaviours and essential for the adaptation, survival and pathogenicity of P. aeruginosa. Abbreviation: CM, cytoplasmic membrane; OM, outer membrane.