Abstract
Acinetobacter baumannii is well adapted to hospital environments, and the persistence of its chronic infections is mainly due to its ability to form biofilms resistant to conventional antibiotics and host immune systems. Hence, the inhibitions of biofilm formation and virulence characteristics provide other means of addressing infections. In this study, the antibiofilm activities of twelve flavonoids were initially investigated. Three most active flavonoids, namely, fisetin, phloretin, and curcumin, dose-dependently inhibited biofilm formation by a reference A. baumannii strain and by several clinical isolates, including four multidrug-resistant isolates. Furthermore, the antibiofilm activity of curcumin (the most active flavonoid) was greater than that of the well-known biofilm inhibitor gallium nitrate. Curcumin inhibited pellicle formation and the surface motility of A. baumannii. Interestingly, curcumin also showed antibiofilm activity against Candida albicans and mixed cultures of C. albicans and A. baumannii. In silico molecular docking of the biofilm response regulator BfmR showed that the binding efficacy of flavonoids with BfmR was correlated with antibiofilm efficacy. In addition, curcumin treatment diminished A. baumannii virulence in an in vivo Caenorhabditis elegans model without cytotoxicity. The study shows curcumin and other flavonoids have potential for controlling biofilm formation by and the virulence of A. baumannii.
Highlights
Most bacteria are able to form biofilms on various biotic and abiotic surfaces, and these films constitute structurally complex systems that defend microbial communities
Drug-resistant biofilm formation appears to play a vital role in the pathogenicity of A. baumannii (Qi et al, 2016), and biofilm development is critically dependent on the assembly of the csuA/BABCDE chaperon–usher, whereas pili production is required for adhesion to abiotic surfaces (Pakharukova et al, 2018)
In A. baumannii it has been reported that biofilm formation and pili production were abolished by inactivation of the csuE gene (Tomaras et al, 2003), and that biofilm formation and motility are under the direct control of the two-component response regulator BfmR, which acts as a master control switch for biofilm development (Russo et al, 2016)
Summary
Most bacteria are able to form biofilms on various biotic and abiotic surfaces, and these films constitute structurally complex systems that defend microbial communities. Drug-resistant biofilm formation appears to play a vital role in the pathogenicity of A. baumannii (Qi et al, 2016), and biofilm development is critically dependent on the assembly of the csuA/BABCDE chaperon–usher, whereas pili production is required for adhesion to abiotic surfaces (Pakharukova et al, 2018). In A. baumannii it has been reported that biofilm formation and pili production were abolished by inactivation of the csuE gene (Tomaras et al, 2003), and that biofilm formation and motility are under the direct control of the two-component response regulator BfmR, which acts as a master control switch for biofilm development (Russo et al, 2016)
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