Abstract
Infections caused by antibiotic-resistant strains of Staphylococcus aureus have reached epidemic proportions globally. Staphylococcal biofilms are associated with increased antimicrobial resistance and are generally less affected by host immune factors. Therefore, there is an urgent need for novel agents that not only aim at multidrug-resistant pathogens, but also ones that will act as anti biofilms. In the present study, we investigated the antimicrobial activity of the endocannabinoid (EC) anandamide (AEA) and the endocannabinoid-like (EC-like), arachidonoyl serine (AraS) against methicillin resistant S. aureus strains (MRSA). We observed a strong inhibition of biofilm formation of all tested MRSA strains as well as a notable reduction of metabolic activity of pre-formed MRSA biofilms by both agents. Moreover, staphylococcal biofilm-associated virulence determinants such as hydrophobicity, cell aggregation and spreading ability were altered by AEA and AraS. In addition, the agents were able to modify bacterial membrane potential. Importantly, both compounds prevent biofilm formation by altering the surface of the cell without killing the bacteria. Therefore, we propose that EC and EC-like compounds may act as a natural line of defence against MRSA or other antibiotic resistant bacteria. Due to their anti biofilm action these agents could also be a promising alternative to antibiotic therapeutics against biofilm-associated MRSA infections.
Highlights
Infectious diseases have been associated with morbidity and mortality throughout the history of mankind
Another means for bacteria to evolve resistance to antibiotics is a single or poly-mutational event leading to overexpression of a multidrug-resistance mechanism, i.e., an efflux pump, or genes encoding a specific drug-deactivating enzyme[3]
Using the standard broth microdilution methods, we evaluated the minimal inhibitory concentration (MIC) of the tested compounds
Summary
Infectious diseases have been associated with morbidity and mortality throughout the history of mankind. A multidrug-resistant phenotype can arise in bacteria through the acquisition of multiple acquired resistance mechanisms due to environmental pressure These resistance factors can stem from mobile genetic elements, a combination of acquired and chromosomally encoded resistance mechanisms, or accumulation of multiple chromosomal changes over time. Another means for bacteria to evolve resistance to antibiotics is a single or poly-mutational event leading to overexpression of a multidrug-resistance mechanism, i.e., an efflux pump, or genes encoding a specific drug-deactivating enzyme[3]. In addition to the increasing prevalence and incidence of community-associated methicillin-resistant S. aureus (CA-MRSA), the strains appear to be especially virulent[8]. MRSA can colonize the health care units of hospitals and clinics[10,11,12] and are of specific public danger
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