Persister cells

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Persister cells are subpopulations of cells that resist treatment, and become antimicrobial tolerant by changing to a state of

cancer drugs.[6]

History

Recognition of bacterial persister cells dates back to 1944 when

culture medium with the penicillin-treated liquid. Colonies of bacteria were able to grow after antibiotic exposure. The important observation that Bigger made was that this new population could again be almost eliminated by the use of penicillin except for a small residual population. Hence the residual organisms were not antibiotic resistant mutants but rather a subpopulation of what he called ‘persisters’.[7] The formation of bacterial persisters is now known to be a common phenomenon that can occur by the formation of persister cells prior to the antibiotic treatment[8] or in response to a variety of antibiotics.[9]

Relevance to chronic infections

Antimicrobial tolerance is achieved by a small subpopulation of microbial cells termed persisters.

pathogenic microbes cannot be eliminated by the immune system, they become a reservoir from which recurrence of infection will develop.[10] Such non-growing bacteria have been observed to persist during infections from Salmonella.[11] Persister cells are the main cause of relapsing and chronic infections.[2][5]

The bacteria species Listeria monocytogenes, the main causal agent of listeriosis, has been shown to demonstrate persistence during infection in hepatocyte and trophoblast cells. The usual active lifestyle can change and the bacteria can remain in intracellular vacuoles entering into a slow non-growing state of persistence thus promoting their survival from antibiotics.[12]

Fungal persister cells are a common cause of recurring infections due to Candida albicans a common biofilm infection of implants.[5]

Medical importance

Further information: Biofilm § In medicine

Antibiotic tolerance poses medically important challenges. It is largely responsible for the inability to eradicate bacterial infections with antibiotic treatment. Persister cells are highly enriched in biofilms, and this makes biofilm-related diseases difficult to treat. Examples are chronic infections of implanted medical devices such as catheters and artificial joints, urinary tract infections, middle ear infections and fatal lung disease.[13]

Resistance vs tolerance

Unlike

sensitive to antibiotics.[2][7][10]

Molecular mechanisms

The molecular mechanisms that underlie persister cell formation, and antimicrobial tolerance are largely unknown.

envelope stress response,[17] and the starvation response have also been associated with persister cell formation in biofilms.[18] Owing to their transient nature and relatively low abundance, it is hard to isolate persister cells in sufficient numbers for experimental characterization, and only a few relevant genes have been identified to date.[2][10] The best-understood persistence factor is the E. coli high persistence gene, commonly abbreviated as hipA.[19]

Although tolerance is widely considered a passive state, there is evidence indicating it can be an energy-dependent process.[20] Persister cells in E. coli can transport intracellular accumulations antibiotic using an energy requiring efflux pump called TolC.[21]

A persister subpopulation has also been demonstrated in budding yeast Saccharomyces cerevisiae. Yeast persisters are triggered in a small subset of unperturbed exponentially growing cells by spontaneously occurring DNA damage, which leads to the activation of a general stress response and protection against a range of harsh drug and stress environments. As a result of the DNA damage, yeast persisters are also enriched for random genetic mutations that occurred prior to the stress, and are unrelated to the stress survival.[22]

In response to antifungals, fungal persister cells activate stress-response pathways, and two stress-protective molecules – glycogen, and trehalose accumulate in large amounts.[5]

Potential treatment

A study has shown that adding certain

E. coli and S. aureus.[23]

Phage therapy, where applicable, entirely circumvents antibiotic tolerance.[24][25]

See also

References

  1. PMID 28333307
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  2. ^
    S2CID 6670040
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  3. ^
    S2CID 8308100
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  4. ^
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  5. ^
    PMID 30335865
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  6. S2CID 53285399
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  7. ^
    doi:10.1016/S0140-6736(00)74210-3
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  8. S2CID 39698842
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  9. PMID 20528688
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  10. ^
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  11. PMID 24408438
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  12. PMID 29190284
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  14. PMID 19054118
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  18. S2CID 10216159
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  25. PMID 37257734
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External links
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