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Effects of Vibrio Cholerae Protease and Pigment Production on Environmental Survival and Host Interaction

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Effects of Vibrio Cholerae Protease and Pigment Production on Environmental Survival and Host Interaction Effects of Vibrio cholerae protease and pigment production on environmental survival and host interaction Karolis Vaitkevičius Department of Molecular Biology Umeå University Umeå 2007 1 Department of Molecular Biology Umeå University SE-90187 Umeå Sweden Copyright © 2007 by Karolis Vaitkevičius ISSN 0346-6612 ISBN 978-91-7264-464-9 Printed by Print & Media, Umeå University, Umeå, 2007 2 Table of content Abstract ......................................................................................................................................................... 5 Main articles of this thesis ............................................................................................................................ 6 Introduction .................................................................................................................................................. 7 1. Cholera background .............................................................................................................................. 7 1.1. Serological classification of V. cholerae ......................................................................................... 8 2. Virulence factors of Vibrio cholerae and their biological function...................................................... 10 2.1. Cholera toxin ................................................................................................................................ 10 2.2 Toxin co-regulated pili (TCP) ......................................................................................................... 10 2.3. Vibrio cytolysin (VCC/HlyA) .......................................................................................................... 11 2.4. RTX toxin....................................................................................................................................... 13 2.5. Mannose sensitive hemagglutinin ............................................................................................... 14 3. Regulation of V. cholerae virulence factors ........................................................................................ 16 4. Protein secretion systems in Gram-negative bacteria ........................................................................ 21 4.1. TAT translocation pathway .......................................................................................................... 21 4.2. Sec secretion pathway ................................................................................................................. 22 4.3. Type I, or ABC (ATP-binding cassette) exporters.......................................................................... 23 4.4. Type II secretion system ............................................................................................................... 23 4.5. Type III, contact dependent secretion system ............................................................................. 23 4.6. Type IV secretion system ............................................................................................................. 25 4.7. Type V. Autotransporters and proteins requiring single accessory factors ................................. 26 4.8. Chaperone/usher pathway .......................................................................................................... 27 4.9. Type VI secretion system ............................................................................................................. 27 5. V. cholerae-host interaction models ................................................................................................... 30 5.1. Mammalian infection models ...................................................................................................... 30 5.2. Non-mammalian infection models ............................................................................................... 30 3 6. Innate Immunity in C. elegans ............................................................................................................. 33 6.1. Evasion strategy ........................................................................................................................... 33 6.2. Physical barriers ........................................................................................................................... 33 6.3. Signalling pathways regulating immune responses in C. elegans ................................................ 33 6.4. Effector molecules of C. elegans innate immunity ...................................................................... 35 7. Peptidases ........................................................................................................................................... 37 7.1. Proteolysis in pathogenesis and host interactions ....................................................................... 37 7.2. Processing of extracellular proteases .......................................................................................... 40 8. Secreted V. cholerae peptidases ......................................................................................................... 41 8.1. Hemagglutinin/protease .............................................................................................................. 41 8.2. Vibrio aminopeptidase ................................................................................................................. 42 8.3. The PrtV protease ......................................................................................................................... 43 9. Bacterial melanins and pathogenesis .................................................................................................. 46 Aims of the thesis ........................................................................................................................................ 48 Results and Discussion ................................................................................................................................ 49 Article I .................................................................................................................................................... 49 Article II ................................................................................................................................................... 52 Article III .................................................................................................................................................. 55 Article IV .................................................................................................................................................. 57 Conclusions ................................................................................................................................................. 59 Acknowledgements ..................................................................................................................................... 60 References ................................................................................................................................................... 62 Articles I-IV .................................................................................................................................................. 74 4 Abstract Only two out of more than 200 V. cholerae serogroups, classified on the basis of LPS structure, are associated with epidemic or pandemic cholera. These toxigenic serogroups carry phage-derived pathogenicity islands coding for the main virulence factors for establishment of cholera disease – cholera toxin (CTX) and toxin-coregulated pilus (TCP). The latter also serves as a bacterial surface receptor for the CTXΦ – the filamentous phage which carries the cholera toxin genes into otherwise harmless to human, environmental bacterium V. cholerae. In its natural aquatic habitat V. cholerae is subject to predator grazing, bacteriophage killing, temperature and pH changes, seasonality of plankton blooms and other environmental factors. Therefore understanding V. cholerae pathogenic and virulence potential requires the knowledge of its interaction not only with human host but also members of aquatic environment and environmental factors. V. cholerae is capable of killing the nematode Caenorhabditis elegans. Using a reverse genetics approach, we demonstrated that the quorum sensing regulated protease PrtV is essential for this killing. Other proteases did not seem to contribute to virulence in this model. The data from this study suggest that the PrtV could be important to V. cholerae in its natural niche for its resistance to the grazing predators. The PrtV protease belongs to an M6 family of metallopeptidases which is represented by an Immune Inhibitor A protease from the insect killing bacterium Bacillus thuringiensis. To characterize the protease in more detail, the PrtV was cloned, overexpressed in V. cholerae and purified from the culture supernatant. The enzyme was calcium stabilized and inhibited by metal ion chelators. In tests with in vitro cultured cells of the human intestinal cell line HCT8, the PrtV protein showed a cytotoxic effect leading to cell detachment and death. Using human blood plasma as a source of potential substrates, and by tests with purified candidate substrate proteins, we have identified fibrinogen (all α, β and γ chains), fibronectin and plasminogen to be degraded by the protease. Additionally, PrtV was found to alter the stability of V. cholerae
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