Aims: Bacterial biofilms generally are more resistant to stresses as compared with free planktonic cells. Therefore, the discovery of antimicrobial stress factors that have strong inhibitory effects on bacterial biofilm formation would have great impact on the food, personal care, and medical industries.
Methods and Results: Salicylate‐based poly(anhydride esters) (PAE) have previously been shown to inhibit biofilm formation, possibly by affecting surface attachment. Our research evaluated the effect of salicylate‐based PAE on biofilm‐forming Salmonella enterica serovar Typhimurium. To remove factors associated with surface physical and chemical parameters, we utilized a strain that forms biofilms at the air–liquid interface. Surface properties can influence biofilm characteristics, so the lack of attachment to a solid surface eliminates those constraints. The results indicate that the salicylic acid‐based polymers do interfere with biofilm formation, as a clear difference was seen between bacterial strains that form biofilms at the air–liquid interface (top‐forming) and those that form at the surface–liquid interface (bottom‐forming).
Conclusion: These results lead to the conclusion that the polymers may not interfere with attachment; rather, the polymers likely affect another mechanism essential for biofilm formation in Salmonella.
Significance and Impact of the study: Biofilm formation can be prevented through controlled release of nature‐derived antimicrobials formulated into polymer systems.
Recent reports indicate the presence of autoinducer‐2 (AI‐2)‐like activity in foods such as milk and tofu; it is unclear what effect this molecule may have on virulence and survivability of foodborne pathogens. Quorum sensing has been implicated in stress responses of certain bacteria, and in this study we investigated AI‐2‐mediated quorum sensing as one of the mechanisms through which the general stress response in Listeria monocytogenes could be triggered. In particular, the ability of L. monocytogenes to acquire resistance to the food preservatives nisin and lactic acid was examined. The cells were pre‐exposed to extracellular AI‐2 and then challenged with the specific stresses so the level of adaptation caused by the pre‐exposure could be assessed. Our data suggested that the resistance to the studied antimicrobials was not mediated through AI‐2‐dependent quorum sensing pathways. No evidence was found suggesting that quorum sensing in general was involved in L. monocytogenes response to stress.
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