Abstract

As a facultative intracellular pathogen, Salmonella Enteritidis must develop an effective oxidative stress response to survive exposure to reactive oxygen species within the host. To study this defense mechanism, we carried out a series of oxidative stress assays in parallel with a comparative transcriptome analyses using a next generation sequencing approach. It was shown that the expression of 45% of the genome was significantly altered upon exposure to H2O2. Quantitatively the most significant (≥100 fold) gene expression alterations were observed among genes encoding the sulfur utilization factor of Fe-S cluster formation and iron homeostasis. Our data point out the multifaceted nature of the oxidative stress response. It includes not only numerous mechanisms of DNA and protein repair and redox homeostasis, but also the key genes associated with osmotic stress, multidrug efflux, stringent stress, decrease influx of small molecules, manganese and phosphate starvation stress responses. Importantly, this study revealed that oxidatively stressed S. Enteritidis cells simultaneously repressed key motility encoding genes and induced a wide range of adhesin- and salmonellae-essential virulence-encoding genes, that are critical for the biofilm formation and intracellular survival, respectively. This finding indicates a potential intrinsic link between oxidative stress and pathogenicity in non-typhoidal Salmonella that needs to be empirically evaluated.

Highlights

  • Non-typhoidal Salmonella is a leading cause of foodborne gastroenteritis on the global scale

  • It has been estimated that from 2000 to 2008, non-typhoidal Salmonella serovars accounted for 1.2 million laboratory-confirmed illnesses, 19,000 hospitalizations, and 380 deaths each year in the USA [2]

  • This study employing a combination of incremental oxidative stress assays and the generation sequencing approach revealed additional levels of the oxidative stress response complexity in non-typhoidal Salmonella

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Summary

Introduction

Non-typhoidal Salmonella is a leading cause of foodborne gastroenteritis on the global scale. This foodborne pathogen is responsible for 80 million cases of gastroenteritis annually [1]. The situation in the USA is very similar to the global epidemiological picture of salmonellosis caused by non-typhoidal Salmonella. It has been estimated that from 2000 to 2008, non-typhoidal Salmonella serovars accounted for 1.2 million laboratory-confirmed illnesses, 19,000 hospitalizations, and 380 deaths each year in the USA [2]. The high incidence rate is made more significant by the fact that there have been no signs of decline in the incidence of salmonellosis over the past 15 years in the US. Infections caused by other five major food-borne pathogens (i.e., Escherichia coli O157:H7, Campylobacter spp., Listeria monocytogenes, Yersinia enterocolitica, and Shigella spp.) declined substantially over the same time [2]

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