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Background  Tigecycline resistance in  Acinetobacter baumannii  is primarily acquired through overexpression of the AdeABC efflux pump. Besides AdeRS, other two-component regulatory systems (TCSs) involving the regulation of this transporter have not been clarified.    Results  In this study, we found that the TCS genes  baeR  and  baeS  are co-transcribed and function as stress responders under high osmotic conditions. The  baeSR  and  adeAB  genes showed increased transcription in both the laboratory-induced and clinical tigecycline-resistant strains compared with the wild-type strain. The deletion of  baeR  in the ATCC 17978 strain led to 67–73% and 68% reduction in  adeA  and  adeB  expression, respectively, with a resultant 2-fold decrease in the tigecycline minimal inhibition concentration (MIC). In contrast, the overexpression of  baeR  resulted in a doubled tigecycline MIC, with a more than 2-fold increase in  adeA  and  adeB  expression. The influence of  baeR  knockout on  adeAB  gene expression can also be observed in the laboratory-induced tigecycline-resistant strain. A time-kill assay showed that the  baeR  deletion mutant showed an approximate 1-log 10  reduction in colony forming units (CFUs) relative to the wild-type strain when the tigecycline concentration was 0.25 μg/mL throughout the assay period. The wild-type phenotype could be restored by trans-complementation with pWH1266- kan    r   - baeR . Increasing the tigecycline concentration to 0.5 μg/mL produced an even more marked 4.7-log 10  reduction in CFUs of the  baeR  deletion mutant at 8 h, while only a 2.1-log 10  reduction was observed for the wild-type strain.    Conclusions  Taken together, these data show for the first time that the BaeSR TCS influences the tigecycline susceptibility of  A. baumannii  through the positive regulation of the resistance-nodulation-division efflux pump genes  adeA  and  adeB .

Role of the BaeSR two-component system in the regulation of Acinetobacter baumannii adeAB genes and its correlation with tigecycline susceptibility