Inhibitory effects of nafcillin and diosmin on biofilm formation by Salmonella Typhimurium.

Objective: The foodborne pathogen Salmonella enterica serovar Typhimurium causes self-limiting gastroenteritis in humans and is difficult to eliminate due to its ability to adhere to surfaces and form biofilms that exhibit high resistance to antimicrobial agents. To explore alternative strategies for biofilm treatment, it is essential to investigate novel agents that inhibit Salmonella biofilms.
Method: In this study, we investigated the minimum biofilm inhibitory concentrations (MBICs) and minimum biofilm eradication concentrations (MBECs) of nafcillin and diosmin, both previously identified as Lon protease inhibitors, against biofilms formed by S. Typhimurium. Furthermore, we examined the expression of genes associated with the type II toxin-antitoxin system to enhance our understanding of the impact of these inhibitors.
Results: The findings indicated a strong antibiofilm effect of nafcillin, with MBIC and MBEC values of 8 µg/mL and 32 µg/mL, respectively. These results were confirmed by field emission scanning electron microscopy (FE-SEM), which showed that biofilm formation was reduced in the presence of nafcillin. Additionally, it revealed morphological changes in the bacteria within the nafcillin-treated biofilms. Furthermore, gene expression analyses demonstrated a significant reduction in the expression of type II TA system genes following treatment with nafcillin and diosmin.
Conclusion: This study highlights the effectiveness of nafcillin in disrupting the biofilms of S. Typhimurium. These results suggest promising avenues for the development of novel therapeutic strategies targeting biofilms associated with S. Typhimurium.
Competing Interests: Declarations. Ethical approval: This study was approved by the Ethics Committee of Iran University of Medical Sciences by Ethics No. (IR.IUMS.FMD.REC.1402.262). Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.
(© 2024. The Author(s).)