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  • Title: Effects of aerobactin-encoding gene iucB and regulator of mucoid phenotype rmpA on the virulence of Klebsiella pneumoniae causing liver abscess.
    Author: Liu S, Huang Z, Kong J, Zhao Y, Xu M, Zhou B, Zheng X, Ye D, Zhou T, Cao J, Zhou C.
    Journal: Front Cell Infect Microbiol; 2022; 12():968955. PubMed ID: 36439210.
    Abstract:
    This study aimed to analyze the influence of the main aerobactin-encoding gene iucB and the regulator of mucoid phenotype rmpA on the virulence of Klebsiella pneumoniae causing liver abscess. In addition, the possible regulatory effects of the main encoding gene iucB on the regulator of mucoid phenotype rmpA were explored, thus providing novel strategies for the prevention and control of hypervirulent K. pneumoniae (hvKp) causing liver abscess. The virulence-related genes iucB and rmpA of K. pneumoniae were detected by PCR. iucB and rmpA were cloned into K. pneumoniae strain by using plasmid pET28b as vector. Quantitative real-time PCR (RT-qPCR) was employed to detect the relative expression of rmpA gene in K. pneumoniae. We investigated the potential effects of aerobactin coding gene iucB and regulator of mucoid phenotype rmpA on the virulence of K. pneumoniae by establishing the Galleria mellonella infection model. Capsule quantitative experiment was conducted to investigate the impact of aerobactin-encoding gene iucB on the modulation of regulator of mucoid phenotype rmpA. The results of the G. mellonella infection model indicated that iucB gene could significantly enhance the virulence of K. pneumoniae, but the presence of rmpA gene did not markedly affect the virulence of K. pneumoniae. RT-qPCR showed that iucB inhibited the expression of rmpA gene. Quantitative capsulation experiments showed that the presence of rmpA gene could not increase the capsulation production of K. pneumoniae. The main encoding gene of aerobactin, namely iucB, could substantially enhance the virulence of K. pneumoniae. The gene iucB might be involved in the biosynthesis of the capsular polysaccharide through an unknown mechanism instead of the gene rmpA. Overall, these findings provide important theoretical support for the treatment of infections caused by hvKp.
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