Dataset Information

Vibrio vulnificus RtxA1 Toxin Expression Upon Contact With Host Cells Is RpoS-Dependent.

ABSTRACT: The expression of virulence genes in bacteria is known to be regulated by various environmental and host factors. Vibrio vulnificus, an estuarine bacterium, experiences a dramatic environmental change during its infection process. We reported that V. vulnificus RtxA1 toxin caused acute cell death only when close contact to host cells was allowed. A sigma factor RpoS is a very important regulator for the maximal survival of pathogens under stress conditions. Here, we studied the role of RpoS in V. vulnificus cytotoxicity and mouse lethality. The growth of rpoS mutant strain was comparable to that of wild-type in heart infusion (HI) media and DMEM with HeLa cell lysate. An rpoS mutation resulted in decreased cytotoxicity, which was restored by in trans complementation. Interestingly, host contact increased the expression and secretion of V. vulnificus RtxA1 toxin, which was decreased and delayed by the rpoS mutation. Transcription of the cytotoxic gene rtxA1 and its transporter rtxB1 was significantly increased after host factor contact, whereas the activity was decreased by the rpoS mutation. In contrast, the rpoS mutation showed no effect on the transcriptional activity of a cytolytic heamolysin gene (vvhA). Additionally, the LD50 of the rpoS mutant was 15-fold higher than that of the wild-type in specific pathogen-free CD-1 female mice. Taken together, these results show that RpoS regulates the expression of V. vulnificus RtxA1 toxin and its transporter upon host contact.

SUBMITTER: Guo RH

PROVIDER: S-EPMC5862816 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Vibrio vulnificus RtxA1 Toxin Expression Upon Contact With Host Cells Is RpoS-Dependent.

Guo Rui Hong RH Lim Ju Young JY Tra My Duong Nu DN Jo Se Jin SJ Park Jung Up JU Rhee Joon Haeng JH Kim Young Ran YR

Frontiers in cellular and infection microbiology 20180315

The expression of virulence genes in bacteria is known to be regulated by various environmental and host factors. Vibrio vulnificus, an estuarine bacterium, experiences a dramatic environmental change during its infection process. We reported that V. vulnificus RtxA1 toxin caused acute cell death only when close contact to host cells was allowed. A sigma factor RpoS is a very important regulator for the maximal survival of pathogens under stress conditions. Here, we studied the rol ...[more]

PMID: 29600196

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Project description:To understand toxin-stimulated host-pathogen interactions, we performed dual-transcriptome sequencing experiments using human epithelial (HT-29) and differentiated THP-1 (dTHP-1) immune cells infected with the sepsis-causing pathogen Vibrio vulnificus (either the wild-type [WT] pathogen or a multifunctional-autoprocessing repeats-in-toxin [MARTX] toxin-deficient strain). Gene set enrichment analyses revealed MARTX toxin-dependent responses, including negative regulation of extracellular related kinase 1 (ERK1) and ERK2 (ERK1/2) signaling and cell cycle regulation in HT-29 and dTHP-1 cells, respectively. Further analysis of the expression of immune-related genes suggested that the MARTX toxin dampens immune responses in gut epithelial cells but accelerates inflammation and nuclear factor κB (NF-κB) signaling in immune cells. With respect to the pathogen, siderophore biosynthesis genes were significantly more highly expressed in WT V. vulnificus than in the MARTX toxin-deficient mutant upon infection of dTHP-1 cells. Consistent with these results, iron homeostasis genes that limit iron levels for invading pathogens were overexpressed in WT V. vulnificus-infected dTHP-1 cells. Taken together, these results suggest that MARTX toxin regulates host inflammatory responses during V. vulnificus infection while also countering host defense mechanisms such as iron limitation.IMPORTANCEV. vulnificus is an opportunistic human pathogen that can cause life-threatening sepsis in immunocompromised patients via seafood poisoning or wound infection. Among the toxic substances produced by this pathogen, the MARTX toxin greatly contributes to disease progression by promoting the dysfunction and death of host cells, which allows the bacteria to disseminate and colonize the host. In response to this, host cells mount a counterattack against the invaders by upregulating various defense genes. In this study, the gene expression profiles of both host cells and V. vulnificus were analyzed by RNA sequencing to gain a comprehensive understanding of host-pathogen interactions. Our results suggest that V. vulnificus uses the MARTX toxin to subvert host cell immune responses as well as to oppose host counterattacks such as iron limitation.

Dataset Information

Vibrio vulnificus RtxA1 Toxin Expression Upon Contact With Host Cells Is RpoS-Dependent.

Publications

<i>Vibrio vulnificus</i> RtxA1 Toxin Expression Upon Contact With Host Cells Is RpoS-Dependent.

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