A Genetically Tractable, Natural Mouse Model of Cryptosporidiosis Offers Insights into Host Protective Immunity

Adam Sateriale, Jan Šlapeta, Rodrigo Baptista, Julie B. Engiles, Jodi A. Gullicksrud, Gillian T. Herbert, Carrie F. Brooks, Emily M. Kugler, Jessica C. Kissinger, Christopher A. Hunter, B. Striepen

    Research output: Contribution to journalArticlepeer-review

    59 Scopus citations

    Abstract

    Cryptosporidium is a leading cause of diarrheal disease and an important contributor to early childhood mortality, malnutrition, and growth faltering. Older children in high endemicity regions appear resistant to infection, while previously unexposed adults remain susceptible. Experimental studies in humans and animals support the development of disease resistance, but we do not understand the mechanisms that underlie protective immunity to Cryptosporidium. Here, we derive an in vivo model of Cryptosporidium infection in immunocompetent C57BL/6 mice by isolating parasites from naturally infected wild mice. Similar to human cryptosporidiosis, this infection causes intestinal pathology, and interferon-γ controls early infection while T cells are critical for clearance. Importantly, mice that controlled a live infection were resistant to secondary challenge and vaccination with attenuated parasites provided protection equal to live infection. Both parasite and host are genetically tractable and this in vivo model will facilitate mechanistic investigation and rational vaccine design.

    Original languageEnglish (US)
    Pages (from-to)135-146.e5
    JournalCell Host and Microbe
    Volume26
    Issue number1
    DOIs
    StatePublished - Jul 10 2019

    Keywords

    • Apicomplexa
    • Cryptosporidium
    • cryptosporidiosis
    • diarrhea
    • host-pathogen
    • immunity
    • intestine
    • parasite

    ASJC Scopus subject areas

    • Parasitology
    • Microbiology
    • Virology

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