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Published on: February 9, 2011
Effects of prolonged exposure to diclofenac sodium on strains of Staphylococcus aureus
A A de Lima-E-Silva1, R G da Silva-Filho1, A S Viana1,2
1Universidade Federal do Estado do Rio de Janeiro, Instituto Biomédico, Departamento de Microbiologia e Parasitologia, Laboratório de Biologia e Fisiologia de Microrganismos, Rio de Janeiro, RJ, Brasil.
Abstract:
Staphylococcus aureus is a pathogen commonly involved in the etiology of nosocomial and community-acquired infections. This microorganism adheres and forms biofilm on biotic and abiotic surfaces, which is a significant complication for infection control. More recently, non-antibiotic medications, such as nonsteroidal anti-inflammatory agents (NSAIDs), have been studied as an alternative for treating infections caused by multidrug-resistant pathogens and infections associated with biofilms. This study assessed the effects of prolonged exposure of S. aureus strains to the NSAID diclofenac sodium regarding biofilm production, direct adhesion, hydrophobicity, susceptibility to antimicrobials, hemolysis, and biochemical profile. Some strains exposed to diclofenac showed increased direct adhesion to hydrophobic and hydrophilic surfaces and increased cell surface hydrophobicity. Two strains, one reference and one clinical, were subjected to repeated and prolonged passages in a culture medium with a diclofenac gradient. In one of them, the drug suppressed biofilm production in the assay with and without subinhibitory concentrations (sub-MICs) from NSAID. Additional repeated passages of this strain in a medium without diclofenac partially recovered the original biofilm-positive phenotype, but only in culture with sub-MICs of the drug. The original characteristics of the strains regarding susceptibility or resistance to antimicrobials and biochemical profile were not affected by prolonged exposure to diclofenac. However, the clinical isolate showed suppressed hemolytic activity.
Insights
Prolonged exposure to diclofenac sodium, a nonsteroidal anti-inflammatory drug (NSAID), altered Staphylococcus aureus adhesion and biofilm formation. Some strains showed increased adhesion and hydrophobicity, while one strain
Area of Science:
- Microbiology
- Infectious Diseases
- Pharmacology
Background:
- Staphylococcus aureus is a major cause of hospital and community infections.
- Biofilm formation by S. aureus complicates infection control and treatment.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are being explored for treating resistant bacterial infections and biofilms.
Purpose of the Study:
- To investigate the effects of prolonged exposure to diclofenac sodium on S. aureus.
- To assess changes in biofilm production, adhesion, hydrophobicity, antimicrobial susceptibility, hemolysis, and biochemical profile.
Main Methods:
- S. aureus strains were subjected to prolonged exposure to diclofenac sodium.
- Assays evaluated biofilm production, direct adhesion to surfaces, and cell surface hydrophobicity.
- Susceptibility to antimicrobials, hemolytic activity, and biochemical profiles were also analyzed.
Main Results:
- Diclofenac exposure increased direct adhesion and cell surface hydrophobicity in some S. aureus strains.
- One strain showed suppressed biofilm production after prolonged diclofenac exposure, with partial recovery upon drug removal.
- Antimicrobial susceptibility and biochemical profiles remained unaffected; hemolytic activity was suppressed in a clinical isolate.
Conclusions:
- Prolonged exposure to diclofenac sodium can alter S. aureus adhesion and biofilm formation.
- Diclofenac may influence bacterial surface properties and virulence factors like hemolysis.
- Further research is needed to understand the therapeutic potential of NSAIDs against S. aureus biofilms.
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