Siderophore iucA of hypermucoviscous Klebsiella pneumoniae promotes liver damage in mice by inducing oxidative stress

The hypermucoviscosity/hypervirulent K. pneumoniae (hvKP) is a dominant cause of pyogenic liver abscess (PLA) and has contributed to the endemicity of disease in Asian country. The siderophore aerobactin (iucA) is highly expressed in hvKP and acting virulence role during hvKP infection. However, its role in the PLA is poorly understood. We constructed iucA deletion mutant (Delta iucA-hvKP852) and used animal study to characterize the role of siderophore iucA in K. pneumoniae liver abscess. The animal experiments showed that Delta iucA-hvKP852 strain had lower virulence in mice compared to hvKP852 wild type strain. At 24 h after infection, only two of ten mice developed liver abscess during infection with Delta iucA-hvKP852 strain, while nine of ten mice infected with wild type hvKP852 strain showed multiple lesions of liver abscess. The liver tissue infected with Delta iucA-hvKP852 exhibited low reactive oxygen stress levels compared to those infected by wild type hvKP852 strain (P < 0.05). The results suggest that siderophore iucA play an important role in the liver abscess by inducing oxidative stress.

Automated summary

The siderophore aerobactin (iucA) plays an important role in the formation of pyogenic liver abscess caused by hypermucoviscosity/hypervirulent K. pneumoniae (hvKP). This study showed that iucA deletion led to decreased virulence of hvKP852 strain in mice and reduced reactive oxygen stress levels in liver tissue, indicating the significance of iucA in the pathogenesis of liver abscess.