Abstract
The increasing threat of Acinetobacter baumannii as a nosocomial pathogen is mainly due to the occurrence of multidrug-resistant strains that are associated with the real problem of its eradication from hospital wards. The particular ability of this pathogen to form biofilms contributes to its persistence, increases antibiotic resistance, and promotes persistent/device-related infections. We previously demonstrated that virstatin, which is a small organic compound known to decrease virulence of Vibrio cholera via an inhibition of T4-pili expression, displayed very promising activity to prevent A. baumannii biofilm development. Here, we examined the antibiofilm activity of mono-unsaturated chain fatty acids, palmitoleic (PoA), and myristoleic (MoA) acids, presenting similar action on V. cholerae virulence. We demonstrated that PoA and MoA (at 0.02 mg/mL) were able to decrease A. baumannii ATCC 17978 biofilm formation up to 38% and 24%, respectively, presented a biofilm dispersing effect and drastically reduced motility. We highlighted that these fatty acids decreased the expression of the regulator abaR from the LuxIR-type quorum sensing (QS) communication system AbaIR and consequently reduced the N-acyl-homoserine lactone production (AHL). This effect can be countered by addition of exogenous AHLs. Besides, fatty acids may have additional non-targeted effects, independent from QS. Atomic force microscopy experiments probed indeed that PoA and MoA could also act on the initial adhesion process in modifying the material interface properties. Evaluation of fatty acids effect on 22 clinical isolates showed a strain-dependent antibiofilm activity, which was not correlated to hydrophobicity or pellicle formation ability of the tested strains, and suggested a real diversity in cell-to-cell communication systems involved in A. baumannii biofilm formation.
Highlights
Acinetobacter baumannii is a bacterial pathogen causing nosocomial outbreaks worldwide and is responsible for many infections, such as pneumonia and bloodstream infections, especially in intensive cares units [1,2]
Addition of PoA reduced significantly the biofilm formation at the three tested concentrations, whereas MoA exhibited a significant activity only at 0.02 and 0.05 mg/mL. These results showed that unsaturated fatty acids (UFAs) display a biofilm inhibition activity that is similar to that of virstatin, for which the decrease reached 32%, MoA being less active than PoA at lower concentrations
To further examine the activity of UFAs and virstatin on acyl-homoserine lactone production (AHL) production, we evaluated the activity of these compounds on the A. baumannii biofilm formation in presence of 500 nM of the main AHLs already described, i.e., OH-C12-HSL or N-C10-HSL [13,14,15] (Figure 2b)
Summary
Acinetobacter baumannii is a bacterial pathogen causing nosocomial outbreaks worldwide and is responsible for many infections, such as pneumonia and bloodstream infections, especially in intensive cares units [1,2]. World Health Organization to classify A. baumannii among the “Critical” bacterial agents (priority 1), for which research and development of new and effective antibiotic treatments are urgently required This pathogen is problematic for its long-time survival in hospital settings owing to its great ability to survive desiccation [3] or treatment with disinfectants [4]. Some mono-unsaturated fatty acids (UFAs) as palmitoleic (cis-9-hexadecenoïc, C16:1∆9, PoA) and myristoleic (cis-9-tetradecenoïc, C14:1∆9, MoA) acids were shown to inhibit tcp genes expression in V. cholerae [16,17]. These molecules prevent the interaction between their transcriptional regulator ToxT and the DNA [18]. We evaluated the efficacy of unsaturated fatty acids, PoA and MoA, as antibiofilm compounds and investigated their effect on A. baumannii QS system
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