AIM: To analyze the expression and regulation of resistance-nodulation-division (RND) efflux systems in clinical tigecycline-nonsusceptible (TNS) Acinetobacter baumannii. MATERIALS & METHODS: Comparisons of molecular and clinical characteristics were performed between 52 TNS and 53 tigecycline-susceptible isolates. Expression of RND efflux pumps and global regulators were analyzed by real-time RT-PCR. A complementation experiment was performed to evaluate the contribution of the adeRS mutations. RESULTS: Mechanical ventilation and prior use of carbapenems were more common among patients with TNS strains. The relative expression of adeB and adeJ was increased significantly in TNS isolates. Complementarity to the adeR or adeS mutations decreased tigecycline susceptibility by ≤2-fold. Decreased expression of marR and soxR was detected in TNS isolates. CONCLUSION: A correlation between tigecycline MIC and expression level of adeB and adeJ was identified. The influence of adeRS mutation on adeB expression was limited. Global regulators marR and soxR may be involved in tigecycline resistance.
AIM: To analyze the expression and regulation of resistance-nodulation-division (RND) efflux systems in clinical tigecycline-nonsusceptible (TNS) Acinetobacter baumannii. MATERIALS & METHODS: Comparisons of molecular and clinical characteristics were performed between 52 TNS and 53 tigecycline-susceptible isolates. Expression of RND efflux pumps and global regulators were analyzed by real-time RT-PCR. A complementation experiment was performed to evaluate the contribution of the adeRS mutations. RESULTS: Mechanical ventilation and prior use of carbapenems were more common among patients with TNS strains. The relative expression of adeB and adeJ was increased significantly in TNS isolates. Complementarity to the adeR or adeS mutations decreased tigecycline susceptibility by ≤2-fold. Decreased expression of marR and soxR was detected in TNS isolates. CONCLUSION: A correlation between tigecycline MIC and expression level of adeB and adeJ was identified. The influence of adeRS mutation on adeB expression was limited. Global regulators marR and soxR may be involved in tigecycline resistance.