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Colonization of fish skin is vital for Vibrio anguillarum to cause disease
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology). (Debra L. Milton)
Department of Applied Marine Biology, LMB and LAMB of South China Sea Institute of Oceanography.
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology).
2010 (English)In: Environmental Microbiology Reports, ISSN 1758-2229, Vol. 2, no 1, 133-139 p.Article in journal (Refereed) Published
Abstract [en]

Vibrio anguillarum causes a fatal haemorrhagic septicaemia in marine fish. During initial stages of infection, host surfaces are colonized; however, few virulence factors required for colonization of the host are identified. In this study, in vivo bioluminescent imaging was used to analyse directly the colonization of the whole rainbow trout animal by V. anguillarum. The wild type rapidly colonized both the skin and the intestines by 24 h; however, the bacterial numbers on the skin were significantly higher than in the intestines indicating that skin colonization may be important for disease to occur. Mutants defective for the anguibactin iron uptake system, exopolysaccharide transport, or Hfq, an RNA chaperone, were attenuated for virulence, did not colonize the skin, and penetrated skin mucus less efficiently than the wild type.These mutants, however, did colonize the intestines and were as resistant to 2% bile salts as is the wildtype. Moreover, exopolysaccharide mutants were significantly more sensitive to lysozyme and antimicrobial peptides, while the Hfq and anguibactin mutants were sensitive to lysozyme compared with the wildtype. Vibrio anguillarum encodes several mechanisms to protect against antimicrobial components of skin mucus enabling an amazingly abundant growth on the skin enhancing its disease opportunities.

Place, publisher, year, edition, pages
Society for Applied Microbiology and Blackwell Publishing Ltd. , 2010. Vol. 2, no 1, 133-139 p.
Keyword [en]
Vibrio anguillarum, skin colonization, vibriosis
National Category
Microbiology in the medical area
Research subject
URN: urn:nbn:se:umu:diva-33156DOI: 10.1111/j.1758-2229.2009.00120.xISI: 000279431900019OAI: diva2:310230
Available from: 2010-04-13 Created: 2010-04-13 Last updated: 2010-04-27Bibliographically approved
In thesis
1. Stress response and virulence in Vibrio anguillarum
Open this publication in new window or tab >>Stress response and virulence in Vibrio anguillarum
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Bacteria use quorum sensing, a cell to cell signaling mechanism mediated by small molecules that are produced by specific signal molecule synthases, to regulate gene expression in response to population density. In Vibrio anguillarum, the quorum-sensing phosphorelay channels information from three hybrid sensor kinases VanN, VanQ, CqsS that sense signal molecules produced by the synthases VanM, VanS and CqsA, onto the phosphotransferase VanU, to regulate activity of the response regulator VanO. VanO activates transcription of quorum-sensing regulatory RNAs (Qrr), which work together with the RNA chaperone Hfq to repress expression of the transcriptional regulator VanT.

The work presented in this thesis characterizes quorum-sensing independent and quorum-sensing dependent mechanisms that regulate VanT expression. Moreover, an in vivo imaging system was established, as a means to study V. anguillarum infections in the rainbow trout infection model.

Two quorum-sensing independent mechanisms regulating VanT expression were identified. First, the sigma factor RpoS indirectly activates VanT expression during transition into stationary growth phase by inhibiting hfq expression. Both, RpoS and VanT are crucial for stress response. Second, a type VI secretion system (T6SS) has a novel function as a signal sensing mechanism to regulate rpoS and vanT expression. Consequently, RpoS, quorum sensing and T6SS form a global network that senses stress and modulates stress response to ensure survival of the bacteria.

Further analysis of the quorum-sensing dependent regulation of VanT expression by the phosphorelay system revealed that four qrr genes are expressed continuously during growth. The phosphotransferase VanU is suggested to activate two response regulators, VanO and a predicted second response regulator. Activated VanO induces expression of the Qrr sRNAs, whereas, the predicted response regulator represses expression of the Qrr sRNAs. Thus, VanU has a pivotal role in the regulation of VanT expression. The signal synthase VanM and VanT form a regulatory loop, in which VanM represses VanT by inducing expression of the Qrr sRNAs and VanT directly activates vanM expression to repress its own expression. Moreover, Hfq destabilizes vanM mRNA, repressing vanM expression. VanT forms another regulatory loop with the transcriptional regulator LuxT, in which LuxT activates vanT expression and VanT directly represses luxT expression.

V. anguillarum is an opportunistic pathogen that causes vibriosis, a terminal hemorrhagic septicemia. The spatial and temporal progression of the infection was analyzed using the whole animal with an in vivo bioluminescent imaging method. Initial studies showed that colonization of the fish skin requires the siderophore, the RNA chaperone Hfq and the exopolysaccharide transport system, which protects against the innate immunity on the skin. Colonization of the fish skin is crucial for disease.

Place, publisher, year, edition, pages
Umeå: Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet) Umeå Universitet, 2010. 86 p.
Vibrio anguillarum, quorum sensing, Type VI secretion, stress response, virulence, skin colonization
National Category
Biochemistry and Molecular Biology
Research subject
Molecular Biology
urn:nbn:se:umu:diva-33269 (URN)978-91-7264-958-3 (ISBN)
Public defence
2010-05-18, NUS, byggnad 6L, Major Groove, Umeå Universitet, Umeå, 13:00 (English)
Available from: 2010-04-27 Created: 2010-04-20 Last updated: 2011-03-14Bibliographically approved

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Weber, BarbaraMilton, Debra L.
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