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    Immune-driven alterations in mucin sulphation is an important mediator of Trichuris muris helminth expulsion

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    Author
    Hasnain, SZ; Dawson, PA; Lourie, R; Hutson, P; Tong, H; Grencis, RK; McGuckin, MA; Thornton, DJ
    Date
    2017-02-01
    Source Title
    PLoS Pathogens
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    McGuckin, Michael
    Affiliation
    Medicine Dentistry & Health Sciences
    Metadata
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    Document Type
    Journal Article
    Citations
    Hasnain, S. Z., Dawson, P. A., Lourie, R., Hutson, P., Tong, H., Grencis, R. K., McGuckin, M. A. & Thornton, D. J. (2017). Immune-driven alterations in mucin sulphation is an important mediator of Trichuris muris helminth expulsion. PLOS PATHOGENS, 13 (2), https://doi.org/10.1371/journal.ppat.1006218.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/255559
    DOI
    10.1371/journal.ppat.1006218
    Abstract
    Mucins are heavily glycosylated proteins that give mucus its gel-like properties. Moreover, the glycans decorating the mucin protein core can alter the protective properties of the mucus barrier. To investigate whether these alterations could be parasite-induced we utilized the Trichuris muris (T. muris) infection model, using different infection doses and strains of mice that are resistant (high dose infection in BALB/c and C57BL6 mice) or susceptible (high dose infection in AKR and low dose infection in BALB/c mice) to chronic infection by T. muris. During chronicity, within the immediate vicinity of the T. muris helminth the goblet cell thecae contained mainly sialylated mucins. In contrast, the goblet cells within the epithelial crypts in the resistant models contained mainly sulphated mucins. Maintained mucin sulphation was promoted by TH2-immune responses, in particular IL-13, and contributed to the protective properties of the mucus layer, making it less vulnerable to degradation by T. muris excretory secretory products. Mucin sulphation was markedly reduced in the caecal goblet cells in the sulphate anion transporter-1 (Sat-1) deficient mice. We found that Sat-1 deficient mice were susceptible to chronic infection despite a strong TH2-immune response. Lower sulphation levels lead to decreased efficiency of establishment of T. muris infection, independent of egg hatching. This study highlights the complex process by which immune-regulated alterations in mucin glycosylation occur following T. muris infection, which contributes to clearance of parasitic infection.

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