Quorum Sensing as a Target for Controlling Surface Associated Motility and Biofilm Formation in ATCC 17978.

The important nosocomial pathogen presents a quorum sensing (QS) system (/) mediated by acyl-homoserine-lactones (AHLs) and several quorum quenching (QQ) enzymes. However, the roles of this complex network in the control of the expression of important virulence-related phenotypes such as surface-associated motility and biofilm formation is not clear. Therefore, the effect of the mutation of the AHL synthase AbaI, and the exogenous addition of the QQ enzyme Aii20J on surface-associated motility and biofilm formation by ATCC 17978 was studied in detail. The effect of the enzyme on biofilm formation by several multidrug-resistant clinical isolates differing in their motility pattern was also tested. We provide evidence that a functional QS system is required for surface-associated motility and robust biofilm formation in ATCC 17978. Important differences were found with the well-studied strain M2 regarding the relevance of the QS system depending on environmental conditions The biofilm-formation capacity of clinical strains was highly variable and was not related to the antibiotic resistance or surface-associated motility profiles. A high variability was also found in the sensitivity of the clinical strains to the action of the QQ enzyme, revealing important differences in virulence regulation between isolates and confirming that studies restricted to a single strain are not representative for the development of novel antimicrobial strategies. Extracellular DNA emerges as a key component of the extracellular matrix in biofilms since the combined action of the QQ enzyme Aii20J and DNase reduced biofilm formation in all tested strains. Results demonstrate that QQ strategies in combination with other enzymatic treatments such as DNase could represent an alternative approach for the prevention of colonization and survival on surfaces and the prevention and treatment of infections caused by this pathogen.