Abstract

Stress is an important contributing factor in the outbreak of infectious fish diseases. To comprehensively understand the impact of catecholamine stress hormone norepinephrine (NE) on the pathogenicity of Aeromonas hydrophila, we assessed variations in bacterial growth, virulence‐related genes expression and virulence factors activity after NE addition in serum‐SAPI medium. Further, we assessed the effects of NE on A. hydrophila virulence in vivo by challenging fish with pathogenic strain AH196 and following with or without NE injection. The NE‐associated stimulation of A. hydrophila strain growth was not linear‐dose‐dependent, and only 100 μM, or higher concentrations, could stimulate growth. Real‐time PCR analyses revealed that NE notably changed 13 out of the 16 virulence‐associated genes (e.g. ompW, ahp, aha, ela, ahyR, ompA, and fur) expression, which were all significantly upregulated in A. hydrophila AH196 (p < 0.01). NE could enhance the protease activity, but not affect the lipase activity, hemolysis, and motility. Further, the mortality of crucian carp challenged with A. hydrophila AH196 was significantly higher in the group treated with NE (p < 0.01). Collectively, our results showed that NE enhanced the growth and virulence of pathogenic bacterium A. hydrophila.

Highlights

  • Aeromonas hydrophila is ubiquitously distributed in freshwater habitats, and a well-­known opportunistic pathogen of fish, amphibians, reptiles, and mammals (Altwegg & Geiss, 2008; Pang et al, 2015; Parker & Shaw, 2011)

  • Recent researches have suggested that stress hormones can significantly influence the infectivity of pathogenic bacteria (Belay, Aviles, Vance, Fountain, & Sonnenfeld, 2003; Li et al, 2015; Lyte & Ernst, 1992; Neal et al, 2001)

  • We examined the effects of stress hormone NE on the growth, gene expression of selected virulence factors, lytic enzyme activity, hemolysis, and swimming motility of A. hydrophila

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Summary

| INTRODUCTION

Aeromonas hydrophila is ubiquitously distributed in freshwater habitats, and a well-­known opportunistic pathogen of fish, amphibians, reptiles, and mammals (Altwegg & Geiss, 2008; Pang et al, 2015; Parker & Shaw, 2011). Recent researches have suggested that stress hormones can significantly influence the infectivity of pathogenic bacteria (Belay, Aviles, Vance, Fountain, & Sonnenfeld, 2003; Li et al, 2015; Lyte & Ernst, 1992; Neal et al, 2001). The catecholamine stress hormone NE is mainly released from sympathetic nerve terminals, and maintains a highly conserved molecular structure in vertebrates including fish, amphibians, and mammals (Freestone, Haigh, & Lyte, 2007; Nakano, Takahashi, Sakai, Kawano, et al, 2007). NE was found to affect the production of virulence factors in pathogens, including the motility of Salmonella enterica serovar Typhimurium (Bearson & Bearson, 2008), Escherichia coli O157:H7 (Bansal et al, 2007) and Vibrio harveyi (Yang, Anh, Bossier, & Defoirdt, 2014), and biofilm formation of Staphylococcus epidermidis (Lyte et al, 2003), Vibrio harveyi (Yang et al, 2014), and Streptococcus pneumonia (Sandrini, Alghofaili, Freestone, & Yesilkaya, 2014). We evaluated the impact of NE on the virulence of A. hydrophila in crucian carp Carassius auratus gibelio via in vivo challenge

| MATERIALS AND METHODS
| DISCUSSION
Findings
CONFLICT OF INTEREST
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