Antibiotics Promote Escherichia coli-Pseudomonas aeruginosa Conjugation through Inhibiting Quorum Sensing [PublishAheadOfPrint]

The effect of antibiotics on horizontal gene transfer is controversial and the underlying mechanism remains poorly understood. Here, using E. coli SM10 which carries a chromosomally integrated RP4 plasmid as donor strain, we investigated the effect of antibiotics on conjugational transfer of a mobilizable gentamicin (Gm) resistance plasmid. The results showed that exposure to gentamicin that may restrict the survival of recipient cells significantly enhanced SM10-P. aeruginosa (PAO1) conjugation, which was attenuated by deficiency of lasI/rhlI, genes associated with generation of the quorum sensing signals N-acyl homoserine lactones (AHLs) in PAO1, or deletion of the AHLs receptor SdiA in SM10. Subsequent mechanism investigations revealed that treatment with Gm repressed the mRNA expression of lasI and rhlI in PAO1 and upregulated traI expression in SM10. Moreover, PAO1 treated with other QS-inhibitory antibiotics such as azithromycin or chloramphenicol also showed conjugation-promoting ability. On the other hand, when using non-AHLs- producing E. coli strain EC600 as recipient cells, the promoting effect of Gm on conjugation could not be observed. These data suggest that AHLs-SdiA contributes to the effectiveness of antibiotics on plasmid conjugation. Collectively, our findings highlight the HGT-promoting effect of antibiotics and suggest quorum sensing as a promising target for controlling antibiotic resistance dissemination. These findings have implications for assessing the risks of antibiotic use and developing advisable antibiotic treatment protocols.

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