About this Research Topic
Persisters are phenotypic variants of regular cells in bacterial populations and are highly tolerant to multiple antibiotics. Persisters remain in a dormant state and are able to survive high doses of antibiotic treatment. Upon removal of antibiotics, persisters start to grow like regular cells as a consequence of phenotypic switching. Toxin/antitoxin systems play a major role in the formation of persisters. Activation of toxins put cells into dormancy by various mechanisms including: interfering with replication, translation and decreasing the proton motive force. Formation of persister cells are influenced by growth phases and environmental stresses. Persister cells are much more abundant in biofilm than in planktonic culture, the matrix of which shield persister cells from host immune cells.
Persister cells are thought to be responsible for recurrent and chronic infections, which pose a significant threat to public health. Therefore, it is urgent to fully understand the formation and physiology of persister cells and to develop medicines and strategies for the eradication of persister cells.
Studies on the mechanism of persistence, regulation or function of toxin/antitoxin systems, inducing signals of persister formation, experimental systems to study persister cells, survival mechanisms of persister in host as well as new strategies to combat persisters will be compiled in this Research Topic. Submissions can be made in any format, including original research articles, perspectives, opinions, and reviews.
Keywords: bacterial persisters, toxin/antitoxin system, gene regulation, chronic infection, treatment strategy
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