Edwardsiella tarda – Virulence mechanisms of an emerging gastroenteritis pathogen

Leung, Ka Yin; Siame, Bupe A.; Tenkink, Byron Joel; Noort, Rebecca; Mok, Yu Keung

doi:10.1016/j.micinf.2011.08.005

Cited by 196 publications

(148 citation statements)

References 61 publications

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“…In a recent study of the ocean metagenome (Persson et al, 2009) the T6SS was more abundant among -proteobacteria than other protein transport systems. The weight of present evidence suggests, at least indirectly, an apparently rampant lateral transfer of T6SS clusters/genes in the microbial world, which could be a significant driver for newly emerging pathogens, as proposed for the gastroenteritis agent E. tarda (Leung et al, 2011).…”

Section: Prospectsmentioning

confidence: 70%

Phytobacterial Type VI Secretion System - Gene Distribution, Phylogeny, Structure and Biological Functions

Sarris¹,

Trantas²,

Skandalis³

et al. 2012

Plant Pathology

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Section: Prospectsmentioning

confidence: 70%

Phytobacterial Type VI Secretion System - Gene Distribution, Phylogeny, Structure and Biological Functions

Sarris¹,

Trantas²,

Skandalis³

et al. 2012

Plant Pathology

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“…11,12 A better understanding of E. piscicida pathogenesis may make it possible to produce an appropriate and effective vaccine to prevent edwardsiellosis. Several virulence factors have been reported to be involved in the pathogenesis of this bacterium, including T3SS, which enables it to escape phagocytic killing and to replicate intracellularly in phagocytes, 22 and T6SS, which also contributes to the establishment of colonization inside the host.…”

Section: Discussionmentioning

confidence: 99%

“…4 Edwardsiella piscicida (formerly included in E. tarda), 5,6,7,8 a member of the Enterobacteriaceae, colonizes a broad range of hosts including fish and mammals and causes fatal hemorrhagic septicemia and gastro-and extra-intestinal infections. 9,10,11,12 As a leading pathogen that threats fresh and seawater aquaculture farms, E. piscicida causes huge economic losses to the world aquaculture industry, especially for farmed flatfish (turbot and flounder). A number of virulence factors are involved in the pathogenesis of this bacterium, including adhesins and temperature-sensitive hemagglutinin (Tsh), which bind to host surfaces and initiate infection, 13,14,15 and EthA hemolysin, which facilitates invasion and the process of internalization into hosts.…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic dissection of the horizontally acquired response regulator EsrB reveals its global regulatory roles in the physiological adaptation and activation of T3SS and the cognate effector repertoire inEdwardsiella piscicidaduring infection toward turbot

et al. 2017

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(2017) Transcriptomic dissection of the horizontally acquired response regulator EsrB reveals its global regulatory roles in the physiological adaptation and activation of T3SS and the cognate effector repertoire in Edwardsiella piscicida during infection toward turbot, Virulence, 8:7, 1355-1377, DOI: 10.1080/21505594.2017 ABSTRACTEdwardsiella piscicida is the leading pathogen threatening worldwide aquaculture industries. The 2-component system (TCS) EsrA-EsrB is essential for the pathogenesis of this bacterium. However, little is known about the regulon and regulatory mechanism of EsrA-EsrB or about the factors that mediate the interaction of TCS with bacterial hosts. Here, our RNA-seq analysis indicated that EsrB strongly induces type III and type VI secretion systems (T3/T6SS) expression and that it modulates the expression of both physiology-and virulence-associated genes in E. piscicida grown in DMEM. EsrB binds directly to a highly conserved 18-bp DNA motif to regulate the expression of T3SS and other genes. EsrB/DMEM-activated genes include 3 known and 6 novel T3SS-dependent effectors. All these effector genes are highly induced by EsrB during the late stage of in vivo infection in fish. Furthermore, although in vivo colonization by the bacterium relies on EsrB and T3/T6SS expression, it does not require the expression of individual effectors other than EseJ. The mutant lacking these 9 effectors showed significant defects in in vivo colonization and virulence toward turbot, and, more importantly, a high level of protection against challenges by wild-type E. piscicida, suggesting that it may represent a promising live attenuated vaccine. Taken together, our data demonstrate that EsrB plays a global regulatory role in controlling physiologic responses and the expression of T3SS and its cognate effector genes. Our findings will facilitate further work on the mechanism of molecular pathogenesis of this bacterium during infection.

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“…E. tarda could live and multiply in macrophages, and escape from the cells. It is important for the bacterium to lead to extra intestinal diseases and systemic infections [6]. E. tarda is capable to detoxify ROS by generating catalase (Kat) and superoxide dismutase (Sod) to survive within macrophages [7,8].…”

Section: Introductionmentioning

confidence: 99%

Deep Sequencing Analysis of the Eha-Regulated Transcriptome of Edwardsiella tarda Following Acidification

Gao¹,

Liu²,

Y³

et al. 2017

Metabolomics

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In response to stresses in host cells, several transcriptional regulators described in E. tarda can activate a series of interacting signaling networks [13]. Our previous study found that Eha is a transcriptional regulator of the MarR family [14]. Eha could also regulate the mRNA levels of some surface structures like the type III secretion system to affect the intracellular survival and virulence of E. tarda [15]. We found that Eha is required for the bacteria to resist oxidative stress and survive in macrophages [16]. As the type III secretion system in E. tarda disturbs the formation of the acidic environment in phagosomes [9], we hypothesized that Eha may be required for the bacteria to resist the acid stress in macrophages.Next generation sequencing technology, RNA-Sequencing (RNAseq), has been used in bacterial transcriptome analyses [17]. We performed a high-throughput RNA-seq study, which has firstly been applied in the transcriptome analyses of E. tarda, to detect and compare the differentially-expressed genes (DEGs) between the ET13 wild type bacterium and its eha mutant following exposure to acid stress. Our present study provides the gene expression profiles and sheds light on the molecular mechanism by which E. tarda survival is regulated by Eha under acid stress conditions. Key words: Eha gene; E. tarda; RNA-seq; Macrophage; Acidification IntroductionEdwardsiella tarda (E. tarda) is a facultative intracellular pathogen that causes Edwardsiellosis in freshwater and marine fish worldwide and a Salmonella-like gastroenteritis in humans [1,2]. Macrophages play critical roles in the defense against invading bacteria. Zhang et al. showed that E. tarda can utilize macrophages as a niche to initiate its virulence and spread systemic infections [3]. However, there are various stressful conditions such as nutrition deprivation, low pH and high reactive oxygen species (ROS) present in the intracellular niche of the phagocytes [4]. There are the strategies that virulent bacterial strains use to evade phagosomes and escape into the cytosol to enable their survival in the cells [5]. E. tarda could live and multiply in macrophages, and escape from the cells. It is important for the bacterium to lead to extra intestinal diseases and systemic infections [6]. E. tarda is capable to detoxify ROS by generating catalase (Kat) and superoxide dismutase (Sod) to survive within macrophages [7,8]. Okuda et al. suggested that the bacterial type III secretion system is able to interfere with the formation of acid stress in phagosomes to facilitate its replication in macrophages [9]. However, little other information is available about how E. tarda is affected by an acidic environment.Some findings have been reported about the changes that occur in other intracellular pathogens in response to acid stress in macrophages. For example, Rathman et al. suggested that an acidic environment in Salmonella-containing phagosomes is necessary for the bacterial survival and replication within the macrophage [10]. Supporting this finding, ...

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Edwardsiella tarda – Virulence mechanisms of an emerging gastroenteritis pathogen

Cited by 196 publications

References 61 publications

Phytobacterial Type VI Secretion System - Gene Distribution, Phylogeny, Structure and Biological Functions

Phytobacterial Type VI Secretion System - Gene Distribution, Phylogeny, Structure and Biological Functions

Transcriptomic dissection of the horizontally acquired response regulator EsrB reveals its global regulatory roles in the physiological adaptation and activation of T3SS and the cognate effector repertoire inEdwardsiella piscicidaduring infection toward turbot

Deep Sequencing Analysis of the Eha-Regulated Transcriptome of Edwardsiella tarda Following Acidification

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