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Klebsiella pneumoniae  is an important human pathogen known for its resistance to carbapenem antibiotics, especially the increasing carbapenem-resistant hypervirulent variants. The carbapenem resistance is mainly caused by the carbapenemase gene  blaKPC  which was commonly found on the IncFII transferable plasmids in  K. pneumoniae  ST11 isolates in regions of China. However, the mechanisms of the plasmid-carrying  blaKPC  regulation by the host strain are not clear. To investigate the chromosome-encoded two-component system (TCS) that regulates the carbapenem resistance of  K. pneumoniae  caused by  blaKPC , twenty-four TCSs of a carbapenem-resistant classical  K. pneumoniae  ST11 clinical isolate were knocked out. The deletion mutation of the TCS regulator  cpxR  exhibited increased sensitivity to carbapenem, which could be restored by complementation with  cpxR in trans . Electrophoretic mobility shift, isothermal titration calorimetry and DNase I footprinting results revealed that CpxR directly bound to the promoter DNA of  blaKPC  and the binding was abolished by disrupting the DNA-binding domain in CpxR. The subsequent  in vivo  assays using the  lacZ  reporter system and qPCR showed that CpxR upregulates the transcription of  blaKPC . Notably, CpxR was also found to activate the transfer of the  blaKPC -carrying IncFII plasmid between the hypervirulent  K. pneumoniae  and  E. coli  isolates, in which CpxR promoted the transcription of the  tra  operon via binding to its promoter region. These results provide an important insight into the regulation of the host factor CpxR in the plasmid-carrying carbapenemase gene in the classical and hypervirulent  K. pneumoniae .

emerging microbes and infections

CpxR promotes the carbapenem antibiotic resistance of  Klebsiella pneumoniae  by directly regulating the expression and the dissemination of  bla                  KPC  on the IncFII conjugative plasmid