Control of nanofiltration membrane biofouling by Pseudomonas aeruginosa using d-tyrosine

Yu, Cong; Wu, Jinjian; Contreras, Alison E.; Li, Qilin

doi:10.1016/j.memsci.2012.08.051

Cited by 61 publications

(18 citation statements)

References 27 publications

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“…The destructive effect of non-canonical D-amino acids on biofilms is a well-known phenomenon, first demonstrated when D-amino acids were identified as selfproduced disassembling factors in aging B. subtilis biofilms (Kolodkin-Gal et al, 2010;Oppenheimer-Shaanan et al, 2013). Non-canonical D-amino acids have been shown independently to inhibit biofilm formation and trigger biofilm disassembly in different model organisms (Hochbaum et al, 2011;Yu et al, 2012;Sanchez et al, 2013;Li and Wang, 2014;Si et al, 2014;Xing et al, 2015), and at concentrations that did not interfere with planktonic growth. Importantly, it was reported that B. subtilis NCIB 3610 (as well as many other natural isolates; Daligault et al, 2014) is carrying a defective allele of the dtd gene, involved in removal of D-amino acids from tRNA.…”

Section: Discussionmentioning

confidence: 99%

Disturbance of the bacterial cell wall specifically interferes with biofilm formation

Bucher

Oppenheimer-Shaanan

Savidor

et al. 2015

Environ Microbiol Rep

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In nature, bacteria communicate via chemical cues and establish complex communities referred to as biofilms, wherein cells are held together by an extracellular matrix. Much research is focusing on small molecules that manipulate and prevent biofilm assembly by modifying cellular signalling pathways. However, the bacterial cell envelope, presenting the interface between bacterial cells and their surroundings, is largely overlooked. In our study, we identified specific targets within the biosynthesis pathways of the different cell wall components (peptidoglycan, wall teichoic acids and teichuronic acids) hampering biofilm formation and the anchoring of the extracellular matrix with a minimal effect on planktonic growth. In addition, we provide convincing evidence that biofilm hampering by transglycosylation inhibitors and D-Leucine triggers a highly specific response without changing the overall protein levels within the biofilm cells or the overall levels of the extracellular matrix components. The presented results emphasize the central role of the Gram-positive cell wall in biofilm development, resistance and sustainment.

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Section: Discussionmentioning

confidence: 99%

Disturbance of the bacterial cell wall specifically interferes with biofilm formation

Bucher

Oppenheimer-Shaanan

Savidor

et al. 2015

Environ Microbiol Rep

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“…D-amino acids may stimulate biofilm disassembly in B. subtilis (36) and inhibit biofilm formation of Pseudomonas aeruginosa (37, 38), Staphylococcus aureus (39) (40), and Staphylococcus epidermidis (41) as well as cause dispersal or detachment of cells from single-species and multi-species biofilms containing P. aeruginosa (42), S. epidermidis (41), or Staphylococcus aureus (43, 44). D-amino acids may inhibit adhesion of bacterial cells to one another (45, 46).…”

Section: Introductionmentioning

confidence: 99%

Bacterial d -amino acids suppress sinonasal innate immunity through sweet taste receptors in solitary chemosensory cells

et al. 2017

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In the upper respiratory epithelium, bitter and sweet taste receptors present in solitary chemosensory cells influence antimicrobial innate immune defense responses. Whereas activation of the bitter taste receptor (T2R) stimulates surrounding epithelial cells to release antimicrobial peptides, activation of the sweet taste receptor (T1R) in the same cells inhibits this response. It is thought that this mechanism exists to control the magnitude of antimicrobial peptide release based upon the sugar content of airway surface liquid. We hypothesized that D-amino acids, which are produced by various bacteria and activate T1R in taste receptor cells in the mouth, may also activate T1R in the airway. Here, we show that both the T1R2 and T1R3 subunits of the sweet taste receptor (T1R2/3) are present in the same chemosensory cells of primary human sinonasal epithelial cultures. Respiratory isolates of Staphylococcus species, but not Pseudomonas aeruginosa, produced at least two D-amino acids that activate the sweet taste receptor. In addition to inhibiting P. aeruginosa biofilm formation, D-amino acids derived from Staphylococcus inhibited T2R-mediated signaling and defensin secretion in sinonasal cells by activating T1R2/3. D-amino acid–mediated activation of T1R2/3 also enhanced epithelial cell death during challenge with Staphylococcus aureus in the presence of the bitter-receptor–activating compound denatonium benzoate. These data establish a potential mechanism for interkingdom signaling in the airway mediated by bacterial D-amino acids and the mammalian sweet taste receptor in airway chemosensory cells.

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“…D -amino acids compete with D -Alanine for the fifth position in the B. subtilis pentapeptide, and interfere with transpeptidation (Lam et al, 2009; Cava et al, 2011; Lupoli et al, 2011) and transglycosylation (Lam et al, 2009). D -amino acids were found to inhibit and disperse biofilms without affecting planktonic growth in various model organisms (Kolodkin-Gal et al, 2010; Hochbaum et al, 2011; Yu et al, 2012; Sanchez et al, 2013; Li and Wang, 2014; Bucher et al, 2015, 2016; She et al, 2015), but to the best of our knowledge their efficacy on endodontic biofilms was never evaluated.…”

Section: Introductionmentioning

confidence: 92%

Eradication of Enterococcus faecalis Biofilms on Human Dentin

et al. 2016

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Objectives: This work assesses different methods to interfere with Enterococcus faecalis biofilms formed on human dentin slabs.Methods: First, methods are presented that select for small molecule inhibitors of biofilm targets using multi-well polystyrene biofilm plates. Next, we establish methodologies to study and interfere with biofilm formation on a medically relevant model, whereby biofilms are grown on human root dentin slabs.Results: Non-conventional D-amino acid (D-Leucine) can efficiently disperse biofilms formed on dentin slabs without disturbing planktonic growth. Cation chelators interfere with biofilm formation on dentin slabs and polystyrene surfaces, and modestly impact planktonic growth. Strikingly, sodium hypochlorite, the treatment conventionally used to decontaminate infected root canal systems, was extremely toxic to planktonic bacteria, but did not eradicate biofilm cells. Instead, it induced a viable but non-culturable state in biofilm cells when grown on dentin slabs.Conclusion: Sodium hypochlorite may contribute to bacterial persistence. A combination of the methods described here can greatly contribute to the development of biofilm inhibitors and therapies to treat Enterococcus faecalis infections formed in the root canal system.

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Control of nanofiltration membrane biofouling by Pseudomonas aeruginosa using d-tyrosine

Cited by 61 publications

References 27 publications

Disturbance of the bacterial cell wall specifically interferes with biofilm formation

Disturbance of the bacterial cell wall specifically interferes with biofilm formation

Bacterial d -amino acids suppress sinonasal innate immunity through sweet taste receptors in solitary chemosensory cells

Eradication of Enterococcus faecalis Biofilms on Human Dentin

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