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    Induction of virulence factors in Giardia duodenalis independent of host attachment.

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    25
    Author
    Emery, SJ; Mirzaei, M; Vuong, D; Pascovici, D; Chick, JM; Lacey, E; Haynes, PA
    Date
    2016-02-12
    Source Title
    Scientific Reports
    Publisher
    Springer Science and Business Media LLC
    University of Melbourne Author/s
    Emery, Samantha
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Emery, S. J., Mirzaei, M., Vuong, D., Pascovici, D., Chick, J. M., Lacey, E. & Haynes, P. A. (2016). Induction of virulence factors in Giardia duodenalis independent of host attachment.. Sci Rep, 6 (1), pp.20765-. https://doi.org/10.1038/srep20765.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259419
    DOI
    10.1038/srep20765
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751611
    Abstract
    Giardia duodenalis is responsible for the majority of parasitic gastroenteritis in humans worldwide. Host-parasite interaction models in vitro provide insights into disease and virulence and help us to understand pathogenesis. Using HT-29 intestinal epithelial cells (IEC) as a model we have demonstrated that initial sensitisation by host secretions reduces proclivity for trophozoite attachment, while inducing virulence factors. Host soluble factors triggered up-regulation of membrane and secreted proteins, including Tenascins, Cathepsin-B precursor, cystatin, and numerous Variant-specific Surface Proteins (VSPs). By comparison, host-cell attached trophozoites up-regulated intracellular pathways for ubiquitination, reactive oxygen species (ROS) detoxification and production of pyridoxal phosphate (PLP). We reason that these results demonstrate early pathogenesis in Giardia involves two independent host-parasite interactions. Motile trophozoites respond to soluble secreted signals, which deter attachment and induce expression of virulence factors. Trophozoites attached to host cells, in contrast, respond by up-regulating intracellular pathways involved in clearance of ROS, thus anticipating the host defence response.

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