Biofilms are currently defined as structured bacterial communities embedded in a self-produced exopolysaccharide matrix adherent to any abiotic or biological surface. Biofilms are ubiquous, with almost all material coming into contact with naturally occurring fluids being susceptible to this form of bacterial colonization. These communities may be involved in the development of serious human health problems and are also of concern in environmental and industrial settings. Bacterial biofilm infections are particularly problematic because sessile bacteria can withstand host immune responses and are drastically more resistant to antibiotics, biocides and hydrodynamic shear forces than their planktonic counterparts.
One of the most important advantages a biofilm status gives the bacteria is an increased antimicrobial resistance phenotype. Biofilm can be up to 1000-fold more resistant to antibiotics than planktonic cells due to several mechanisms:
• limitation of antibiotic diffusion through the matrix
• transmission of resistance genes within the community can occur through plasmids, transposons and other mobile genetic elements due to the close relationship of the cells, spreading resistance markers
• expression of efflux pumps;
• inactivation of the antibiotic by changes in metal ion concentrations and pH values;
• the presence of persister cells.
Treatment of biofilm-associated infections is a field that requires further study, in part due to the high levels of antibiotic resistance exhibited by biofilm structures conferred in part by the exopolysaccharide matrix.
A revision of the new advances in biofilms research associated with infectious diseases, food industries, environmental and water biofilm as well as a vision of the new strategies to combat them will be compiled in this topic.
Biofilms are currently defined as structured bacterial communities embedded in a self-produced exopolysaccharide matrix adherent to any abiotic or biological surface. Biofilms are ubiquous, with almost all material coming into contact with naturally occurring fluids being susceptible to this form of bacterial colonization. These communities may be involved in the development of serious human health problems and are also of concern in environmental and industrial settings. Bacterial biofilm infections are particularly problematic because sessile bacteria can withstand host immune responses and are drastically more resistant to antibiotics, biocides and hydrodynamic shear forces than their planktonic counterparts.
One of the most important advantages a biofilm status gives the bacteria is an increased antimicrobial resistance phenotype. Biofilm can be up to 1000-fold more resistant to antibiotics than planktonic cells due to several mechanisms:
• limitation of antibiotic diffusion through the matrix
• transmission of resistance genes within the community can occur through plasmids, transposons and other mobile genetic elements due to the close relationship of the cells, spreading resistance markers
• expression of efflux pumps;
• inactivation of the antibiotic by changes in metal ion concentrations and pH values;
• the presence of persister cells.
Treatment of biofilm-associated infections is a field that requires further study, in part due to the high levels of antibiotic resistance exhibited by biofilm structures conferred in part by the exopolysaccharide matrix.
A revision of the new advances in biofilms research associated with infectious diseases, food industries, environmental and water biofilm as well as a vision of the new strategies to combat them will be compiled in this topic.
![Schematic illustration of the regulatory network of surface sensing in Pseudomonas aeruginosa. Upon bacterial attachment to the surface, chemical cues (blue arrows) such as quorum sensing (QS) signals and unknown chemical signals are received by various systems including QS, chemotaxis, and two-component systems (TCSs). Physical contacts (yellow arrows) causing bacterial cell wall stress and retraction of type IV pili (T4P) trigger responding pathways too. Cyclic-di-GMP, the key second messenger for the motile–sessile lifestyle switch, is generated by diguanylate cyclases (orange) and degraded by phosphodiesterases (green). The other second messenger, cAMP, is also involved in the regulation of T4P and flagella biosynthesis. The purple cylinder represents the assembled T4P across the outer membrane (OM) and inner membrane (IM). Phosphorylated proteins are labeled with [scale=0.5]img001. Activation events (black arrowheads) and inhibition events (red T-bars) may be mediated by transcriptional, translational, or post-translational regulatory mechanisms. Dashed arrows or T-bars represent indirect regulation or unknown pathways. Asterisk-labeled FleQ indicates that FleQ plays a dual role as an activator or a repressor in biofilm formation depending on c-di-GMP or ATP binding, respectively.](https://www.frontiersin.org/_rtmag/_next/image?url=https%3A%2F%2Fwww.frontiersin.org%2Ffiles%2FArticles%2F294514%2Ffmicb-08-02671-HTML%2Fimage_m%2Ffmicb-08-02671-g001.jpg&w=3840&q=75)
