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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.
Impact of sodium nitroprusside concentration added to batch cultures of Escherichia coli biofilms on the c-di-GMP levels, morphologies and adhesion of biofilm-dispersed cells
Published in Biofouling, 2022
Ayse Ordek, F. Pinar Gordesli-Duatepe
Previously, Kim and Harshey (2016) reported that diguanylate cyclase (DGC) YfiN protein associated with intracellular c-di-GMP production acts as a division inhibitor in response to cell-envelope stress in E. coli. After the cell expands to divide, it was shown that YfiN settles in the localization area of division proteins and arrests the division process, and the inhibition of the assembly of division proteins causes an increase in bacterial cell size (Weart et al. 2007). In addition, it was also reported that high intracellular c-di-GMP levels are required for mid-cell localization of YfiN in E. coli. Likewise, Schäper et al. (2016) reported that high c-di-GMP levels provoked Sinorhizobium meliloti cell elongation, and the highest c-di-GMP content resulted in the strongest cell elongation. Since the presence of SNP in the medium results in the formation of NO and other RNS which can lead to an increase in the intracellular c-di-GMP level and a possible disruption of the cell envelope by inducing oxidative and/or nitrosative stresses, the observed increase in the length and width of the dispersed cells compared to those of planktonic cells might have been related to the level of their c-di-GMP content together with the degree of envelope stress experienced by the cells.
Bacterial biofilm-derived antigens: a new strategy for vaccine development against infectious diseases
Published in Expert Review of Vaccines, 2021
Abraham Loera-Muro, Alma Guerrero-Barrera, Yannick Tremblay D.N., Skander Hathroubi, Carlos Angulo
Some signaling molecules can be used by bacteria for intra-species and inter-species communications. One of these molecules is the second messenger, cyclic di-GMP (c-di-GMP). In bacteria, c-di-GMP promotes the switch between lifestyles: a sedentary biofilm or a motile free-floating lifestyle [52]. It also affects a wide range of bacterial behaviors, including the cell cycle, motility, fimbrial synthesis, type III secretion, modulation of RNA, stress response, bacterial predation, and virulence [53]. Diguanylate cyclases have a GGDEF domain that generates c-di-GMP from two GTP molecules, whereas phosphodiesterases have a EAL or HD-GYP domain that degrades c-di-GMP to pGpG [54]. Specific c-di-GMP receptor proteins or riboswitch RNAs sense the changes in c-di-GMP levels and regulate specific processes resulting in different phenotypes [53]. Higher diguanylate cyclase activity increases intracellular c-di-GMP levels that stimulate the production of various adhesins and biofilm-associated matrix components resulting in increased adhesion and biofilm formation [52]. On the opposite spectrum, high phosphodiesterase activity reduces the levels of c-di-GMP, which suppresses adhesion leading to biofilm dispersion [54]. For example, Legionella pneumophila, an opportunistic pathogen, uses the second messenger c-di-GMP to regulate an array of bacterial processes that include motility, cell division, differentiation, virulence, as well as biofilm formation [55,56].
Berberine and its structural analogs have differing effects on functional profiles of individual gut microbiomes
Published in Gut Microbes, 2020
Leyuan Li, Lu Chang, Xu Zhang, Zhibin Ning, Janice Mayne, Yang Ye, Alain Stintzi, Jia Liu, Daniel Figeys
Therapeutic drugs can interact with the gut microbiome, leading to changes in drug efficacy and changes in the microbiome which in turn can affect the host.1 Although there is a growing interest in studying drug–microbiome interactions, our understanding of these complex interactions remains limited. It has been proposed that structurally similar compounds would interact with the same enzymes in microbiomes.2 Maier et al. have shown that drugs that are structurally similar had more similar anticommensal activity compared with drugs that were structurally different.3 Similarly, Dutta et al. found that L-captopril and its derivatives are all potential inhibitors of microbial enzyme DapE.4 However, chemically similar compounds can also have markedly different biological actions and activities.5 For example, Wiggers et al. demonstrated that while sulfasalazine inhibited bacterial diguanylate cyclase inhibitor, its two structurally related molecules sulfadiazine and sulfathiazole did not.6 Notably, current structure–activity studies are based on single strains of bacteria. The human gut microbiome is composed of different bacteria, and the composition of the gut microbiome is different between individuals. Therefore, it remains unclear whether structurally similar compounds will affect the gut microbiome in a similar way.