Effects of aerobactin-encoding gene iucB and regulator of mucoid phenotype rmpA on the virulence of Klebsiella pneumoniae causing liver abscess

Abstract

This study aimed to analyze the influence of the main aerobactin-encoding gene <i>iucB</i> and the regulator of mucoid phenotype <i>rmpA</i> on the virulence of <i>Klebsiella pneumoniae</i> causing liver abscess. In addition, the possible regulatory effects of the main encoding gene <i>iucB</i> on the regulator of mucoid phenotype <i>rmpA</i> were explored, thus providing novel strategies for the prevention and control of hypervirulent <i>K. pneumoniae</i> (hvKp) causing liver abscess. The virulence-related genes <i>iucB</i> and <i>rmpA</i> of <i>K. pneumoniae</i> were detected by PCR. <i>iucB</i> and <i>rmpA</i> were cloned into <i>K. pneumoniae</i> strain by using plasmid pET28b as vector. Quantitative real-time PCR (RT-qPCR) was employed to detect the relative expression of <i>rmpA</i> gene in <i>K. pneumoniae</i>. We investigated the potential effects of aerobactin coding gene <i>iucB</i> and regulator of mucoid phenotype <i>rmpA</i> on the virulence of <i>K. pneumoniae</i> by establishing the <i>Galleria mellonella</i> infection model. Capsule quantitative experiment was conducted to investigate the impact of aerobactin-encoding gene <i>iucB</i> on the modulation of regulator of mucoid phenotype <i>rmpA</i>. The results of the <i>G. mellonella</i> infection model indicated that <i>iucB</i> gene could significantly enhance the virulence of <i>K. pneumoniae</i>, but the presence of <i>rmpA</i> gene did not markedly affect the virulence of <i>K. pneumoniae</i>. RT-qPCR showed that <i>iucB</i> inhibited the expression of <i>rmpA</i> gene. Quantitative capsulation experiments showed that the presence of <i>rmpA</i> gene could not increase the capsulation production of <i>K. pneumoniae</i>. The main encoding gene of aerobactin, namely <i>iucB</i>, could substantially enhance the virulence of <i>K. pneumoniae</i>. The gene <i>iucB</i> might be involved in the biosynthesis of the capsular polysaccharide through an unknown mechanism instead of the gene <i>rmpA</i>. Overall, these findings provide important theoretical support for the treatment of infections caused by hvKp.