Triclosan-bacteria interactions: single or multiple target sites?

Escalada, Margarita Gomez; Russell, A. D.; Maillard, Jean‐Yves; Ochs, D.

doi:10.1111/j.1472-765x.2005.01790.x

Cited by 93 publications

(76 citation statements)

References 22 publications

(30 reference statements)

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“…Regardless, there was a major concentration-dependent extension of the lag phase in R. rubrum S1H when it was exposed to triclosan concentrations greater than 10 g/liter. This observation was consistent with the results of a previous study of Escherichia coli, Enterococcus hirae, and Staphylococcus aureus (19). In the present study, the sudden growth of R. rubrum S1H in the presence of triclosan coincided with increased transcription of genes involved in stress resistance mechanisms, efflux pumps, and cell wall consolidation.…”

Section: Discussionsupporting

confidence: 82%

Toxicogenomic Response of Rhodospirillum rubrum S1H to the Micropollutant Triclosan

Pycke

Vanermen

Monsieurs

et al. 2010

Appl Environ Microbiol

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In the framework of the Micro-Ecological Life Support System Alternative (MELiSSA) project, a pilot study was performed to identify the effects of triclosan on the MELiSSA carbon-mineralizing microorganism Rhodospirillum rubrum S1H. Triclosan is a biocide that is commonly found in human excrement and is considered an emerging pollutant in wastewater and the environment. Chronic exposure to MELiSSA-relevant concentrations (>25 g liter ؊1 ) of triclosan resulted in a significant extension of the lag phase of this organism but hardly affected the growth rate. Analytical determinations gave no indication of triclosan biodegradation during the growth experiment, and flow cytometric viability analyses revealed that triclosan is bacteriostatic and only slightly toxic to R. rubrum S1H. Using microarray analyses, the genetic mechanisms supporting the reversibility of triclosan-induced inhibition were scrutinized. An extremely triclosan-responsive cluster of four small adjacent genes was identified, for which there was up to 34-fold induction with 25 g liter ؊1 triclosan. These four genes, for which the designation muf (micropollutant-upregulated factor) is proposed, appear to be unique to R. rubrum and are shown here for the first time to be involved in the response to stress. Moreover, numerous other systems that are associated with the proton motive force were shown to be responsive to triclosan, but they were never as highly upregulated as the muf genes. In response to triclosan, R. rubrum S1H induced transcription of the phage shock protein operon (pspABC), numerous efflux systems, cell envelope consolidation mechanisms, the oxidative stress response, beta-oxidation, and carbonic anhydrase, while there was downregulation of bacterial conjugation and carboxysome synthesis genes. The muf genes and three efflux-related genes showed the most potential to be low-dose biomarkers.

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Section: Discussionsupporting

confidence: 82%

Toxicogenomic Response of Rhodospirillum rubrum S1H to the Micropollutant Triclosan

Pycke

Vanermen

Monsieurs

et al. 2010

Appl Environ Microbiol

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“…Consistent with the analysis of several ENR crystal structures (Lee et al, 2007), the Arabidopsis ligand-binding pocket adjacent to the NAD1 cofactor is composed of hydrophobic residues (Ala-214, Tyr-264, Ile-265, Ala-266, Ile-271, and Phe-246); therefore, the ability of this polar phytotoxin to interact with ENR may be reduced relative to the nonpolar triclosan, although still sufficient to induce electrolyte leakage in the absence of light at high concentrations. Furthermore, the lower clogP of cyperin may hinder its intercalation into the lipid bilayer (relative to triclosan), but may still be involved in the nonspecific perturbation of subcellular membrane structure as was reported with triclosan (Paul et al, 2004;Gomez Escalada et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

A Pathogenic Fungi Diphenyl Ether Phytotoxin Targets Plant Enoyl (Acyl Carrier Protein) Reductase

Dayan

Ferreira²,

Wang³

et al. 2008

Plant Physiology

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Cyperin is a natural diphenyl ether phytotoxin produced by several fungal plant pathogens. At high concentrations, this metabolite inhibits protoporphyrinogen oxidase, a key enzyme in porphyrin synthesis. However, unlike its herbicide structural analogs, the mode of action of cyperin is not light dependent, causing loss of membrane integrity in the dark. We report that this natural diphenyl ether inhibits Arabidopsis (Arabidopsis thaliana) enoyl (acyl carrier protein) reductase (ENR). This enzyme is also sensitive to triclosan, a synthetic antimicrobial diphenyl ether. Whereas cyperin was much less potent than triclosan on this target site, their ability to cause light-independent disruption of membrane integrity and inhibition of ENR is similar at their respective phytotoxic concentrations. The sequence of ENR is highly conserved within higher plants and a homology model of Arabidopsis ENR was derived from the crystal structure of the protein from Brassica napus. Cyperin mimicked the binding of triclosan in the binding pocket of ENR. Both molecules were stabilized by the p-p stacking interaction between one of their phenyl rings and the nicotinamide ring of the NAD 1 . Furthermore, the side chain of tyrosine is involved in hydrogen bonding with a phenolic hydroxy group of cyperin. Therefore, cyperin may contribute to the virulence of the pathogens by inhibiting ENR and destabilizing the membrane integrity of the cells surrounding the point of infection.

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“…For instance, Russell [21] reported that TCS affects many, but not all, types of Gram-positive and Gram-negative bacteria. Inactive bacteria seem to be more resilient to the lethal effects of TCS possibly due to a reduced metabolism and an enhanced physical barrier against TCS created by debris and dead cells in the stationary growth phase [23]. Low TCS concentrations (0.02 -0.5 mg ml 21 ) affected the growth of several bacteria while higher TCS concentrations (5 -50 mg l 21 ) were bactericidal regardless of the growth phase [23].…”

Section: Triclosan -More Than Just Concentrationmentioning

confidence: 99%

“…Inactive bacteria seem to be more resilient to the lethal effects of TCS possibly due to a reduced metabolism and an enhanced physical barrier against TCS created by debris and dead cells in the stationary growth phase [23]. Low TCS concentrations (0.02 -0.5 mg ml 21 ) affected the growth of several bacteria while higher TCS concentrations (5 -50 mg l 21 ) were bactericidal regardless of the growth phase [23]. At higher concentrations, TCS seems to act rapidly and with highly damaging effects to multiple cytoplasmic and membrane targets, resulting in leakage of intracellular material [24].…”

Section: Triclosan -More Than Just Concentrationmentioning

confidence: 99%

The RNA Processing Enzyme Polynucleotide Phosphorylase Negatively Controls Biofi lm Formation by Repressing Poly-N-Acetylglucosamine (PNAG) Production in Escherichia coli C

Sayen¹

2014

Biofilm Control and Antimicrobial Agents

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The accumulation of the widely-used antibacterial and antifungal compound triclosan (TCS) in freshwaters raises concerns about the impact of this harmful chemical on the biofilms that are the dominant life style of microorganisms in aquatic systems. However, investigations to-date rarely go beyond effects at the cellular, physiological or morphological level. The present paper focuses on bacterial biofilms addressing the possible chemical impairment of their functionality, while also examining their substratum stabilization potential as one example of an important ecosystem service. The development of a bacterial assemblage of natural composition -isolated from sediments of the Eden Estuary (Scotland, UK) -on non-cohesive glass beads (,63 mm) and exposed to a range of triclosan concentrations (control, 2 -100 mg L 21 ) was monitored over time by Magnetic Particle Induction (MagPI). In parallel, bacterial cell numbers, division rate, community composition (DGGE) and EPS (extracellular polymeric substances: carbohydrates and proteins) secretion were determined. While the triclosan exposure did not prevent bacterial settlement, biofilm development was increasingly inhibited by increasing TCS levels. The surface binding capacity (MagPI) of the assemblages was positively correlated to the microbial secreted EPS matrix. The EPS concentrations and composition (quantity and quality) were closely linked to bacterial growth, which was affected by enhanced TCS exposure. Furthermore, TCS induced significant changes in bacterial community composition as well as a significant decrease in bacterial diversity. The impairment of the stabilization potential of bacterial biofilm under even low, environmentally relevant TCS levels is of concern since the resistance of sediments to erosive forces has large implications for the dynamics of sediments and associated pollutant dispersal. In addition, the surface adhesive capacity of the biofilm acts as a sensitive measure of ecosystem effects.

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Triclosan-bacteria interactions: single or multiple target sites?

Cited by 93 publications

References 22 publications

Toxicogenomic Response of Rhodospirillum rubrum S1H to the Micropollutant Triclosan

Toxicogenomic Response of Rhodospirillum rubrum S1H to the Micropollutant Triclosan

A Pathogenic Fungi Diphenyl Ether Phytotoxin Targets Plant Enoyl (Acyl Carrier Protein) Reductase

The RNA Processing Enzyme Polynucleotide Phosphorylase Negatively Controls Biofi lm Formation by Repressing Poly-N-Acetylglucosamine (PNAG) Production in Escherichia coli C

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