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Microbial Biofilms
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Chaminda Jayampath Seneviratne, Neha Srivastava, Intekhab Islam, Kelvin Foong and Finbarr Allen
Dispersal is the least understood and perhaps the most complicated process in both fungal and bacterial biofilm development. The trigger for the dispersal process to occur and the biological pathways modulating dispersal may vary considerably among different microorganisms [41]. Cells from the biofilm may detach singly or as a group and move through a fluid phase to seed new sites. Numerous research groups have put forth efforts to understand this mechanism in pathogenic organisms such as P. aeruginosa and C. albicans. Bacterial secondary messengers such as cyclic di-GMP have been shown to provide critical signals for biofilm formation as well as dispersal [42]. The factors which signal dispersion can vary, ranging from environmental stimuli, nutrients, certain chemicals such as cis-2-decenoic acid or nitric oxide or proteins such as BdlA, a chemotaxis regulator [43–45]. It has also been shown recently that phosphorylation status of diguanylate cyclase NIcD can affect the dispersal of biofilms in P. aeruginosa [46]. The aforementioned study demonstrated dispersal inducing environmental cues are sensed by the diguanylate cyclase NicD belonging to a seven transmembrane receptor family. The sensing of dispersal cues by NicD results in NicD dephosphorylation, followed by activation of a chemotaxis regulator BdlA, which in turn activates DipA, a phosphodiesterase molecule. This leads to altered levels of second messenger cyclic-di-GMP molecules signalling dispersion. Studies on C. albicans biofilms have found Set3–NRG1 complex as possible regulators of biofilm dispersal. Set3, an NAD-dependent histone deacetylation complex, modulates NRG, a transcriptional regulator of biofilm dispersal and a repressor of filamentation [47]. The typical dispersal of C. albicans from biofilms is in the yeast form [48]. Moreover, it was shown that deletion of Nrg1 gene in C. albicans attenuates in vivo virulence of the fungus in systemic candidiasis [49]. Therefore, with proper understanding of the dispersal process, alternative therapeutic strategies may be devised for controlling the spread of these pathogenic organisms.
Biofilm and Quorum Sensing inhibitors: the road so far
Published in Expert Opinion on Therapeutic Patents, 2020
Simone Carradori, Noemi Di Giacomo, Martina Lobefalo, Grazia Luisi, Cristina Campestre, Francesca Sisto
Starting from the lipopolysaccharide nature of the microbial biofilms and the ability of fatty acids to disperse preformed biofilms (e.g. cis-2-decenoic acid at 125 μg/mL) [21], the inventors proposed the synthesis of cyclopropane-containing fatty acids resembling the structure of short fatty acids as diffusible signaling factors in bacteria (Figure 4) [22]. The cyclopropane ring was inserted in the position of the double bond of the corresponding monounsaturated fatty acid. These compounds should be able to revert ‘persister’ cells into metabolically active bacteria and thus enhancing the antimicrobial activity of clinically used agents (amikacin, tetracycline, levofloxacin). In addition, they can be linked covalently to biomaterials (chitosan, chitin) in different ratios in order to produce a coated surface where the formation of biofilm is inhibited. Biofilm dispersion measurements were carried out in media containing S. aureus and P. aeruginosa colonies adding after 24 h up to 250 μg/mL of each compound.