Abstract
Many bacteria grow on surfaces forming biofilms. In this structure, they are well protected and often high dosages of antibiotics cannot clear infectious biofilms. The formation and stabilization of biofilms are mediated by diffusible autoinducers (e.g. N-acyl homoserine lactones, small peptides, furanosyl borate diester). Metabolites interfering with this process have been identified in plants, animals and microbes, and synthetic analogues are known. Additionally, this seems to be not the only way to control biofilms. Enzymes capable of cleaving essential components of the biofilm matrix, e.g. polysaccharides or extracellular DNA, and thus weakening the biofilm architecture have been identified. Bacteria also have mechanisms to dissolve their biofilms and return to planktonic lifestyle. Only a few compounds responsible for the signalling of these processes are known, but they may open a completely novel line of biofilm control. All these approaches lead to the destruction of the biofilm but not the killing of the pathogens. Therefore, a combination of biofilm-destroying compounds and antibiotics to handle biofilm infections is proposed. In this article, different approaches to combine biofilm-controlling compounds and antibiotics to fight biofilm infections are discussed, as well as the balance between biofilm formation and virulence.
Highlights
Many bacteria grow on surfaces forming biofilms
This has been shown for E. coli, where both gene expression and phenotype alter in response to acyl-L-homoserine lactones (AHL) of foreign bacteria [32]
These findings show that diffusible signal factors (DSF) similar to AHLs seem to have a rather dedicated role in bacteria-bacteria and even bacteria-fungus interaction, and any medicinal applications for biofilm control will probably focus on the action on a specific pathogen
Summary
Before forming biofilms, bacteria have to synchronize their gene expression in a process called quorum-sensing (QS) [12]. They do this by secreting small extracellular signal molecules acting as autoinducers to start genetic programs [13]. Most bacteria live in multi-species microbial communities, the quorum-sensing signals are received and processed by cells of the same species, and by foreign species [31] This has been shown for E. coli, where both gene expression and phenotype alter in response to AHLs of foreign bacteria [32]. Antibiotic activity has been demonstrated for 3-oxo-dodecanoyl-AHL 6 and is directed against some Gram-positive bacteria, but was not observed for Gram-negative species [36]
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