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    RAGE deficiency predisposes mice to virus-induced paucigranulocytic asthma

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    11
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    Author
    Arikkatt, J; Ullah, MA; Short, KR; Zhang, V; Gan, WJ; Loh, Z; Werder, RB; Simpson, J; Sly, PD; Mazzone, SB; ...
    Date
    2017-01-18
    Source Title
    eLife
    Publisher
    ELIFE SCIENCES PUBLICATIONS LTD
    University of Melbourne Author/s
    Mazzone, Stuart
    Affiliation
    Anatomy and Neuroscience
    Metadata
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    Document Type
    Journal Article
    Citations
    Arikkatt, J., Ullah, M. A., Short, K. R., Zhang, V., Gan, W. J., Loh, Z., Werder, R. B., Simpson, J., Sly, P. D., Mazzone, S. B., Spann, K. M., Ferreira, M. A. R., Upham, J. W., Sukkar, M. B. & Phipps, S. (2017). RAGE deficiency predisposes mice to virus-induced paucigranulocytic asthma. ELIFE, 6, https://doi.org/10.7554/eLife.21199.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258255
    DOI
    10.7554/eLife.21199
    Abstract
    Asthma is a chronic inflammatory disease. Although many patients with asthma develop type-2 dominated eosinophilic inflammation, a number of individuals develop paucigranulocytic asthma, which occurs in the absence of eosinophilia or neutrophilia. The aetiology of paucigranulocytic asthma is unknown. However, both respiratory syncytial virus (RSV) infection and mutations in the receptor for advanced glycation endproducts (RAGE) are risk factors for asthma development. Here, we show that RAGE deficiency impairs anti-viral immunity during an early-life infection with pneumonia virus of mice (PVM; a murine analogue of RSV). The elevated viral load was associated with the release of high mobility group box-1 (HMGB1) which triggered airway smooth muscle remodelling in early-life. Re-infection with PVM in later-life induced many of the cardinal features of asthma in the absence of eosinophilic or neutrophilic inflammation. Anti-HMGB1 mitigated both early-life viral disease and asthma-like features, highlighting HMGB1 as a possible novel therapeutic target.

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