SdiA Enhanced the Drug Resistance of Cronobacter sakazakii and Suppressed Its Motility, Adhesion and Biofilm Formation

Abstract

<i>Cronobacter sakazakii</i> is a common foodborne pathogen, and the mortality rate of its infection is as high as 40-80%. SdiA acts as a quorum sensing regulator in many foodborne pathogens, but its role in <i>C. sakazakii</i> remains unclear. Here, we further determined the effect of the <i>sdiA</i> gene in <i>C. sakazakii</i> pathogenicity. The <i>SdiA</i> gene in <i>C. sakazakii</i> was knocked out by gene editing technology, and the biological characteristics of the Δ<i>sdiA</i> mutant of <i>C. sakazakii</i> were studied, followed by transcriptome analysis to elucidate its effects. The results suggested that <i>SdiA</i> gene enhanced the drug resistance of <i>C. sakazakii</i> but diminished its motility, adhesion and biofilm formation ability and had no effect on its growth. Transcriptome analysis showed that the Δ<i>sdiA</i> upregulated the expression levels of D-galactose operon genes (including <i>dgoR</i>, <i>dgoK</i>, <i>dgoA</i>, <i>dgoD</i> and <i>dgoT</i>) and flagella-related genes (<i>FliA</i> and <i>FliC</i>) in <i>C. sakazakii</i> and downregulated the expression levels of related genes in the type VI secretion system (<i>VasK</i> gene was downregulated by 1.53-fold) and ABC transport system (downregulated by 1.5-fold), indicating that <i>SdiA</i> gene was related to the physiological metabolism of <i>C. sakazakii</i>. The results were useful for clarifying the pathogenic mechanism of <i>C. sakazakii</i> and provide a theoretical basis for controlling bacterial infection.