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    Iron restriction inside macrophages regulates pulmonary host defense against Rhizopus species

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    Author
    Andrianaki, A.M.
    Kyrmizi, I.
    Thanopoulou, K.
    Date
    2018
    Journal
    Nature Communications
    Publisher
    Nature Publishing Group
    Type
    Article
    
    Metadata
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    See at
    https://dx.doi.org/10.1038/s41467-018-05820-2
    Abstract
    Mucormycosis is a life-threatening respiratory fungal infection predominantly caused by Rhizopus species. Mucormycosis has incompletely understood pathogenesis, particularly how abnormalities in iron metabolism compromise immune responses. Here we show how, as opposed to other filamentous fungi, Rhizopus spp. establish intracellular persistence inside alveolar macrophages (AMs). Mechanistically, lack of intracellular swelling of Rhizopus conidia results in surface retention of melanin, which induces phagosome maturation arrest through inhibition of LC3-associated phagocytosis. Intracellular inhibition of Rhizopus is an important effector mechanism, as infection of immunocompetent mice with swollen conidia, which evade phagocytosis, results in acute lethality. Concordantly, AM depletion markedly increases susceptibility to mucormycosis. Host and pathogen transcriptomics, iron supplementation studies, and genetic manipulation of iron assimilation of fungal pathways demonstrate that iron restriction inside macrophages regulates immunity against Rhizopus. Our findings shed light on the pathogenetic mechanisms of mucormycosis and reveal the role of macrophage-mediated nutritional immunity against filamentous fungi. Copyright 2018, The Author(s).
    Keyword
    Mucormycosis
    Rhizopus
    Iron
    Macrophages
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85051929470&doi=10.1038%2fs41467-018-05820-2&partnerID=40&md5=e647d90d63f2f3ec03dbae9c0a83b307; http://hdl.handle.net/10713/9740
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41467-018-05820-2
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    UMB Open Access Articles 2018

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