Antibiotic-induced release of endotoxin from bacteria in vitro

Crosby, Heather A.; Bion, Julian; Penn, Charles W.; Elliott, T. S. J.

doi:10.1099/00222615-40-1-23

Cited by 83 publications

(36 citation statements)

References 24 publications

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“…We hypothesized that following extended ciprofloxacin exposure, the only remaining viable population consists of persister cells, as ciprofloxacin kills and can lyse nonpersister cells (46)(47)(48). Prior to ciprofloxacin treatment or following exposure to saline for 24 h, the vast majority of P. aerugi- …”

Section: Resultsmentioning

confidence: 99%

The Fatty Acid Signaling Molecule cis -2-Decenoic Acid Increases Metabolic Activity and Reverts Persister Cells to an Antimicrobial-Susceptible State

Marques

Morozov

Planzos

et al. 2014

Appl Environ Microbiol

125

112

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bPersister cells, which are tolerant to antimicrobials, contribute to biofilm recalcitrance to therapeutic agents. In turn, the ability to kill persister cells is believed to significantly improve efforts in eradicating biofilm-related, chronic infections. While much research has focused on elucidating the mechanism(s) by which persister cells form, little is known about the mechanism or factors that enable persister cells to revert to an active and susceptible state. Here, we demonstrate that cis-2-decenoic acid (cis-DA), a fatty acid signaling molecule, is able to change the status of Pseudomonas aeruginosa and Escherichia coli persister cells from a dormant to a metabolically active state without an increase in cell number. This cell awakening is supported by an increase of the persister cells' respiratory activity together with changes in protein abundance and increases of the transcript expression levels of several metabolic markers, including acpP, 16S rRNA, atpH, and ppx. Given that most antimicrobials target actively growing cells, we also explored the effect of cis-DA on enhancing antibiotic efficacy in killing persister cells due to their inability to keep a persister cell state. Compared to antimicrobial treatment alone, combinational treatments of persister cell subpopulations with antimicrobials and cis-DA resulted in a significantly greater decrease in cell viability. In addition, the presence of cis-DA led to a decrease in the number of persister cells isolated. We thus demonstrate the ability of a fatty acid signaling molecule to revert bacterial cells from a tolerant phenotype to a metabolically active, antimicrobial-sensitive state. P ersister cells are considered to be a subpopulation of stochastically produced, nongrowing (dormant) cells present in biofilm and planktonic bacterial cultures. Persister cells account for 10 Ϫ6 to 10 Ϫ4 of the total cell population of mid-exponential-phase cells and up to 1% of the total cell population of stationary-phase cells and biofilms, a pattern resembling that of a quorum-sensing mechanism (1-3). Tolerance to antimicrobials is one of the key characteristics of this subpopulation, as persisters escape killing by antimicrobials such as fluoroquinolones, which can kill slowgrowing bacteria but not dormant cells (4). It is therefore not surprising that persister cells are considered to play a major role in the resilience of bacterial populations and have recently been isolated from patients with candidiasis, from cystic fibrosis patients with chronic lung infections, and from Mycobacterium tuberculosis biofilms responsible for chronic tuberculosis (5-8).Several mechanisms have been described to contribute to persister cell formation. For instance, several genes involved in energy generation and cell maintenance have been shown to be downregulated in persister cells, further indicating that persisters are nongrowing, dormant cells (1). Among these genes were members of several operons involved in oxidative phosphorylation, including NADH dehydrogenase, ATP syn...

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Section: Resultsmentioning

confidence: 99%

The Fatty Acid Signaling Molecule cis -2-Decenoic Acid Increases Metabolic Activity and Reverts Persister Cells to an Antimicrobial-Susceptible State

Marques

Morozov

Planzos

et al. 2014

Appl Environ Microbiol

125

112

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“…A particular autolysin tied to killing factors has not yet been identified in gram-negative species. Note that unrelated cidal antibiotics (␤-lactams, aminoglycosides, and fluoroquinolones) may trigger autolysis in gram-negative bacteria (21,33,49,100), although inhibitors of peptidoglycan synthesis produce the most dramatic and complete hydrolysis of the cell wall. It is important to note that even cell wall inhibitors do not always produce a clear-cut picture of lysis when they kill bacteria (29), including cases when killing does depend on the presence of a functional autolysin (95).…”

Section: Genes Controlling Cell Death and Survivalmentioning

confidence: 99%

Programmed Death in Bacteria

Lewis

2000

Microbiol Mol Biol Rev

543

411

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SUMMARY Programmed cell death (PCD) in bacteria plays an important role in developmental processes, such as lysis of the mother cell during sporulation of Bacillus subtilis and lysis of vegetative cells in fruiting body formation of Myxococcus xanthus. The signal transduction pathway leading to autolysis of the mother cell includes the terminal sporulation sigma factor EςK, which induces the synthesis of autolysins CwlC and CwlH. An activator of autolysin in this and other PCD processes is yet to be identified. Autolysis plays a role in genetic exchange in Streptococcus pneumoniae, and the gene for the major autolysin, lytA, is located in the same operon with recA. DNA from lysed cells is picked up by their neighbors and recombined into the chromosome by RecA. LytA requires an unknown activator controlled by a sensory kinase, VncS. Deletion of vncS inhibits autolysis and also decreases killing by unrelated antibiotics. This observation suggests that PCD in bacteria serves to eliminate damaged cells, similar to apoptosis of defective cells in metazoa. The presence of genes affecting survival without changing growth sensitivity to antibiotics (vncS, lytA, hipAB, sulA, and mar) indicates that bacteria are able to control their fate. Elimination of defective cells could limit the spread of a viral infection and donate nutrients to healthy kin cells. An altruistic suicide would be challenged by the appearance of asocial mutants without PCD and by the possibility of maladaptive total suicide in response to a uniformly present lethal factor or nutrient depletion. It is proposed that a low rate of mutation serves to decrease the probability that asocial mutants without PCD will take over the population. It is suggested that PCD is disabled in persistors, rare cells that are resistant to killing, to ensure population survival. It is suggested that lack of nutrients leads to the stringent response that suppresses PCD, producing a state of tolerance to antibiotics, allowing cells to discriminate between nutrient deprivation and unrepairable damage. High levels of persistors are apparently responsible for the extraordinary survival properties of bacterial biofilms, and genes affecting persistence appear to be promising targets for development of drugs aimed at eradicating recalcitrant infections. PCD in unicellular eukaryotes is also considered, including aging in Saccharomyces cerevisiae. Apoptosis-like elimination of defective cells in S. cerevisiae and protozoa suggests that all unicellular life forms evolved altruistic programmed death that serves a variety of useful functions.

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“…The inhibition of DNA replication triggers a bacterial reaction (SOS response), eventually leading to cell death. The SOS response is a particular feature of the action of 4-quinolone and consists of the induction of nonreplicating DNA synthesis and inhibition of cell division leading to filamentation (Mouton and Leroy, 1991;Crosby et al, 1994). Based on our results, the anti-H. pylori activity of WCC is similar to that of fluoroquinolones and is distinct from other antibiotics.…”

Section: Resultsmentioning

confidence: 50%

In Vitro Anti-Helicobacter pylori Activity of Chinese Chive (Allium tuberosum)

Kudo

Takeuchi

Shimamura

et al. 2011

FSTR

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The anti-Helicobacter pylori (H. pylori) activity of a water extract of Chinese chive (Allium tuberosum) (WCC) was investigated. On disk diffusion assay, WCC effectively inhibited the growth of all 21 strains tested, including isogenic mutants, showing inhibition diameters of 12 to 29 mm, irrespective of drug susceptibility and clinical manifestation. The minimum inhibitory concentration (MIC) of WCC was 2.45 mg dry weight/mL. Killing assay with multiples of MIC confirmed that WCC had bactericidal activity and that the inhibitory effects were dose dependent. In addition, to determine whether the inhibitory activity of WCC under severe stress conditions, such as heat and acidity, is altered, the stability of WCC was evaluated. The inhibitory activity of WCC exposed to acidic conditions (pH 1.0 to 6.4) was stable, while heat-treated WCC (100℃, 10 min) showed slightly decreased inhibition activity. On combination assay with antibiotics frequently used in clinical practice, WCC was found to be an innocuous agent for antibiotic activity. These results suggest that daily intake of WCC is able to prevent H. pylori colonization in the stomach, and that it could be applied as adjuvant therapy in H. pylori eradication.Keywords: Helicobacter pylori, Chinese chive, Allium tuberosum, antibiotic resistance, growth inhibition effect, bactericidal activity * To whom correspondence should be addressed. *E-mail: htake@kochi-u.ac.jp (H. Takeuchi) tomokos@kochi-u.ac.jp (T. Shimamura) IntroductionHelicobacter pylori (H. pylori) was recognized as a human carcinogen by IARC in 1994(Sugiyama et al., 2002, and is a pathogenic gram-negative spiral microaerophilic bacterium that colonizes the human stomach in up to half the world's population (Rothenbacher and Brenner, 2003). H. pylori plays a major role in the development of gastro-duodenal diseases, including gastritis, peptic ulcer and gastric cancer, and is associated with a wide range of non-gastrointestinal tract conditions such as idiopathic thrombocytopenic purpura. As gastric cancer is one of the most frequent causes of cancer-related death, eradication of H. pylori can, therefore, contribute to the treatment and prevention of these diseases. Generally, H. pylori infection in clinical practice is treated with an effective regimen, a triple therapy consisting of a proton pump inhibitor and combinations of two antibiotics; amoxicillin (AMPC) and clarithromycin (CAM) or AMPC and metronidazole (MNZ) in Japan (Nishimori, et al., 2006). However, unsuccessful eradication therapy is increasing due to the increased occurrence of drug-resistant H. pylori (Nariman, et al., 2004). The appearance rates of drug-resistant H. pylori against AMPC, CAM and MNZ from 2007to 2009 were 0.4%, 19.4% and 25.7%, respectively (Lyudmila et al., 2010, and these rates are continuing to escalate.Instead of antibiotics, non-antibiotic substances derived from foods with anti-H. pylori activity are now a focus in Gastroenterology. There have been several reports on natural compounds derived from foods, includin...

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Antibiotic-induced release of endotoxin from bacteria in vitro

Cited by 83 publications

References 24 publications

The Fatty Acid Signaling Molecule cis -2-Decenoic Acid Increases Metabolic Activity and Reverts Persister Cells to an Antimicrobial-Susceptible State

The Fatty Acid Signaling Molecule cis -2-Decenoic Acid Increases Metabolic Activity and Reverts Persister Cells to an Antimicrobial-Susceptible State

Programmed Death in Bacteria

In Vitro Anti-Helicobacter pylori Activity of Chinese Chive (Allium tuberosum)

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