Persister cells, dormancy and infectious disease

By Kim Lewis. Nature Reviews Microbiology, 2007

2,055 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Molecular Medicine

View Paper: https://www.semanticscholar.org/paper/25e0b86711b06b4c2524df28e389e763b7fd5c39

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In Genetics

1. Andy Gardner
2. Stuart A. West
3. A. Griffin
4. J. Ghigo
5. C. Beloin
6. D. Lebeaux
7. J. Lennon
8. Stuart E. Jones

In Molecular Biology

1. D. Lebeaux
2. J. Ghigo
3. C. Beloin
4. J. Lennon
5. S. Ha
6. I. Jahid
7. Stuart E. Jones
8. Kim Lewis

In Molecular Medicine

1. J. Ghigo
2. D. Lebeaux
3. C. Beloin
4. Xian-Zhi Li
5. Kim Lewis
6. P. Stewart
7. H. Nikaido
8. M. Franklin

Citations in the corpus

• Physiological heterogeneity in biofilms (2008, background): “Bistability might help to explain the subsets of bacterial cells, called persister cells , that are found in biofilm”
• Assembly and Development of the Pseudomonas aeruginosa Biofilm Matrix (2009, neutral): “are notoriously difficult to eradicate [2,3].”
• Biofilm-Related Infections: Bridging the Gap between Clinical Management and Fundamental Aspects of Recalcitrance toward Antibiotics (2014, methodology): “Thus, the currently proposed model to explain biofilm recalcitrance toward antibiotics relies mainly on the presence of persister cells (13, 14).”
• A review of microbial biofilms of produce: Future challenge to food safety (2012, background): “Significant phenotypic changes in biofilms communities and their resistance to disinfectants may be explained by persister cells (168,169).”
• Metabolite-Enabled Eradication of Bacterial Persisters by Aminoglycosides (2011, neutral): “To further explore this, we tested growth of persisters on the metabolites used for aminoglycoside potentiation, and observed negligible growth of persisters eight hours after metabolite addition (Supplementary Figs 3 and 4).”
• Ciprofloxacin Causes Persister Formation by Inducing the TisB toxin in Escherichia coli (2010, background): “Previous research clearly indicated redundancy in persister formation mechanisms, suggesting a unique design of this cellsurviving function [2].”
• Antibiotic resistance and persistence—Implications for human health and treatment perspectives (2020, neutral): “…including nutrient limitation (Gutierrez et al , 2017), high cell density (Vega et al , 2012), oxidative stress (Wu et al , 2012; Rowe et al , 2020), an acidic environment (Lewis, 2007; Vulin et al , 2018), immune factors (Manina et al , 2015) and exposure to immune cells (Helaine et al , 2014).”
• Dormancy contributes to the maintenance of microbial diversity (2010, background): “Persistor cells, which are capable of surviving antibiotic treatment without resistance mutations, represent one example of this form of dormancy (13).”
• The Social Lives of Microbes (2007, background): “…rise to new populations that have the same vulnerability to antibiotic treatment; and (b) persistence is controlled by a phenotypic switch—all cells have the potential to become persisters and persisters readily revert to normal growth rate (Balaban et al. 2004, Kussell et al. 2005, Lewis 2007).”
• Targeting bacterial membrane function: an underexploited mechanism for treating persistent infections (2010, background): “, and tuberculous granulomas that contain latent Mycobacterium tuberculosis”
• Return of the Trojan horse: intracellular phenotype switching and immune evasion by Staphylococcus aureus (2011, background): “This survival strategy, widespread in bacteria, helps to account for chronic relapsing infections since complete therapeutic eradication is precluded (see Lewis, 2007, for review).”
• Strategies for culture of 'unculturable' bacteria. (2010, background): “Signalling molecules present only within the natural habitat are thought to be essential for the growth of many bacteria (Lewis, 2007; Nichols et al., 2008).”