TY - JOUR
T1 - Interkingdom signal indole inhibits Pseudomonas aeruginosa persister cell waking
AU - Zhang, W.
AU - Yamasaki, R.
AU - Song, S.
AU - Wood, T. K.
N1 - Publisher Copyright:
© 2019 The Society for Applied Microbiology
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Aims: Persister cells are stressed cells that have transient tolerance to antibiotics; these cells undergo no genetic change, but instead, their tolerance is due to reduced metabolism. Unfortunately, little is known about how persisters resuscitate, so we explored the waking of cells in the presence of the interkingdom signal indole. Methods and Results: To generate a large population of persister cells, we induced the persister phenotype in the opportunistic pathogen Pseudomonas aeruginosa by pretreating cells with carbonyl cyanide m-chlorophenylhydrazone to reduce translation by depleting ATP levels, and found, via single cell observations, that proline is sufficient to wake the persister cells. P. aeruginosa is often present in the gastrointestinal tract, and indole from commensal bacteria such as Escherichia coli has been shown to inhibit P. aeruginosa quorum sensing and pathogenicity without influencing growth. Furthermore, indole is not toxic to P. aeruginosa persister cells. However, we find here that physiological concentrations of indole inhibit P. aeruginosa persister cell resuscitation with an efficiency of higher than 95%. Critically, when contacted with E. coli stationary-phase cultures, the indole produced by E. coli completely inhibits persister cell resuscitation of P. aeruginosa. Conclusions: Therefore, E. coli has devised a method to outcompete its competitors by preventing their resuscitation with indole. Significance and Impact of the Study: This work provides insight into why indole is produced by commensal bacteria.
AB - Aims: Persister cells are stressed cells that have transient tolerance to antibiotics; these cells undergo no genetic change, but instead, their tolerance is due to reduced metabolism. Unfortunately, little is known about how persisters resuscitate, so we explored the waking of cells in the presence of the interkingdom signal indole. Methods and Results: To generate a large population of persister cells, we induced the persister phenotype in the opportunistic pathogen Pseudomonas aeruginosa by pretreating cells with carbonyl cyanide m-chlorophenylhydrazone to reduce translation by depleting ATP levels, and found, via single cell observations, that proline is sufficient to wake the persister cells. P. aeruginosa is often present in the gastrointestinal tract, and indole from commensal bacteria such as Escherichia coli has been shown to inhibit P. aeruginosa quorum sensing and pathogenicity without influencing growth. Furthermore, indole is not toxic to P. aeruginosa persister cells. However, we find here that physiological concentrations of indole inhibit P. aeruginosa persister cell resuscitation with an efficiency of higher than 95%. Critically, when contacted with E. coli stationary-phase cultures, the indole produced by E. coli completely inhibits persister cell resuscitation of P. aeruginosa. Conclusions: Therefore, E. coli has devised a method to outcompete its competitors by preventing their resuscitation with indole. Significance and Impact of the Study: This work provides insight into why indole is produced by commensal bacteria.
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U2 - 10.1111/jam.14434
DO - 10.1111/jam.14434
M3 - Article
C2 - 31487414
AN - SCOPUS:85074675114
SN - 1364-5072
VL - 127
SP - 1768
EP - 1775
JO - Journal of Applied Microbiology
JF - Journal of Applied Microbiology
IS - 6
ER -