Abstract
Aeromonas hydrophila is the causative agent of motile Aeromonad septicemia in fish. Previous studies have shown that the myo-inositol metabolism is essential for the virulence of this bacterium. IolR is a transcription inhibitor that negatively regulates myo-inositol metabolic activity. While in the process of studying the inositol catabolism in A. hydrophila Chinese epidemic strain NJ-35, we incidentally found that ΔiolR mutant exhibited obvious autoaggregation and increased biofilm formation compared to the wild type. The role of surface proteins in A. hydrophila autoaggregation was confirmed by different degradation treatments. Furthermore, calcium promotes the formation of aggregates, which disappear in the presence of the calcium chelator EGTA. Transcriptome analysis, followed by targeted gene deletion, demonstrated that biofilm formation and autoaggregation caused by the inactivation of iolR was due to the increased transcription of a RTX-family adhesion gene, rmpA. Further, IolR was determined to directly regulate the transcription of rmpA. These results indicated that iolR is negatively involved in autoaggregation and biofilm formation in A. hydrophila, and this involvement was associated with its inhibition on the expression of rmpA.
Highlights
Aeromonas hydrophila is a gram-negative ubiquitous bacterium that causes infections in humans and a wide variety of aquatic and terrestrial animals[1]
To evaluate the physiological function and pathogenic significance of the inositol metabolism transcriptional regulator IolR in A. hydrophila NJ-35, an iolR gene deletion strain was constructed by homologous recombination
We evaluated bacterial growth in Luria-Bertani broth (LB) medium, and as shown in Fig. 1a, the ΔiolR had a slightly higher optical density than the wild-type strain; both strains entered exponential and stationary phase at the same time indicating no major difference in growth kinetic
Summary
Aeromonas hydrophila is a gram-negative ubiquitous bacterium that causes infections in humans and a wide variety of aquatic and terrestrial animals[1]. The pathogenesis of A. hydrophila is complex and multifactorial, with the involvement of a number of virulence factors, such as adhesins, toxins and iron acquisition systems[2]. New virulence factors are constantly being discovered, the pathogenesis of this bacterium remains unclear. Bacterial pathogens often encounter a limited availability of carbon, nitrogen, and energy sources during infections while competing with other microorganisms for nutrients[3]. Increasing evidence suggests that pathogens have developed specific metabolic strategies to overcome these restrictions to increase their fitness in the nutrient-poor environments[4]. The role of metabolism is increasingly considered important as classical virulence for studying pathogenicity, and metabolic factors required for successful infection are regarded as virulence factors[5]
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