Abstract
Staphylococcus aureus is a pathogen commonly resistant to antibiotics. Biofilm formation is one of the important factors related to its virulence. Non-antibiotics drugs, such as nonsteroidal anti-inflammatory agents (NSAIDs), have been studied as an alternative for treating infections by multiresistant pathogens and biofilm-associated infections. In this study, the effects of NSAID sodium diclofenac on growth inhibition and biofilm formation of S. aureus were evaluated. The minimum inhibitory concentration (MIC) of diclofenac for fifty isolates ranged from 200 to 400 μg/mL. Diclofenac sub-MICs induced biofilm in 32.3% of biofilm-negative strains in tryptic soy broth. All biofilms induced by the drug showed a PIA- (polysaccharide intercellular adhesion-) independent composition, and the scanning electron microscopy showed that the induced biofilm presented a very discrete matrix. The combination of diclofenac with rifampicin sub-MICs induced strong production of PIA-dependent biofilm in three of four strains, while combination of NSAID with NaCl induced the formation of partially polysaccharide biofilm in two strains and PIA-independent biofilm in another strain. The combination of NSAID with glucose resulted in PIA-independent biofilms in all four strains tested. The results showed that diclofenac can commonly induce biofilm production by a PIA-independent pathway. However, when this NSAID is combined with other types of inducing agents, the composition of the biofilm produced may vary.
Highlights
Several drugs have a greater or lesser degree of antibacterial activity, this effect is not their primary therapeutic goal
The increase in the uptake of ethidium bromide by Staphylococcus aureus cells exposed to diclofenac sodium has provided evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) may act by compromising cellular membrane integrity [14]. is drug has induced extensive alterations in the transcriptome of methicillin-resistant S. aureus (MRSA) by changing the expression of hundreds of genes, including those associated with antimicrobial resistance [15]
E literature reports the minimum inhibitory concentration (MIC) of diclofenac for S. aureus with values ranging from 50 to >1000 μg/mL, which may be due to intrinsic physiological characteristics of isolates studied, as well as to the methodological procedures, such as the way for drug solubilization, culture medium, and the technique [8]. e Minimum Bactericidal Concentration (MBC) was detected only at 1600 μg/mL, since plating in TSA of aliquots of wells containing ≤800 μg/ mL resulted in spots with bacterial growth. is result is in contrast with earlier findings, which pointed to a bactericidal action of diclofenac in concentrations lower than 1600 μg/ mL [10, 13, 38, 39]
Summary
Several drugs have a greater or lesser degree of antibacterial activity, this effect is not their primary therapeutic goal. Compounds with these properties are included in medicine classes such antihistamines, statins, antipsychotics, local anesthetics, nonsteroidal anti-inflammatory drugs (NSAIDs) [1], anticonvulsants, and sympatholytic agents [2] and have been called non-antibiotics [3]. Eir antimicrobial action includes bacterial isolates of different species, as well as fungi [5]. Diclofenac (2-[2-[(2,6-dichlorophenyl)amino]phenyl]acetic acid) is a NSAID with an antimicrobial activity in vitro. E antibacterial mechanism of action of diclofenac seems to reside mainly in the inhibition of DNA synthesis [13]. The increase in the uptake of ethidium bromide by Staphylococcus aureus cells exposed to diclofenac sodium has provided evidence that NSAIDs may act by compromising cellular membrane integrity [14]. is drug has induced extensive alterations in the transcriptome of methicillin-resistant S. aureus (MRSA) by changing the expression of hundreds of genes, including those associated with antimicrobial resistance [15]
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