Nucleation of platelets with blood-borne pathogens on Kupffer cells precedes other innate immunity and contributes to bacterial clearance

Connie Hoi Yee Wong, Craig N Jenne, Bjorn Petri, Navina L Chrobok, Paul Kubes

    Research output: Contribution to journalArticleResearchpeer-review

    269 Citations (Scopus)


    Through the use of intravital imaging of the liver, we demonstrate a collaborative role for platelets with Kupffer cells (KCs) in eradicating blood-borne bacterial infection. Under basal conditions, platelets, via the platelet-adhesion receptor GPIb, formed transient touch-and-go interactions with von Willebrand factor (vWF) constitutively expressed on KCs. Bacteria such as Bacillus cereus and methicillin-resistant Staphylococcus aureus (MRSA) were rapidly caught by KCs and triggered platelets to switch from touch-and-go adhesion to sustained GPIIb-mediated adhesion on the KC surface to encase the bacterium. Infected GPIbalpha-deficient mice had more endothelial and KC damage than did their wild-type counterparts, which led to more fluid leakage, substantial polycythemia and rapid mortality. Our study identifies a previously unknown surveillance mechanism by which platelets survey macrophages that rapidly converts to a critical host response to blood-borne bacteria.
    Original languageEnglish
    Pages (from-to)785 - 792
    Number of pages8
    JournalNature Immunology
    Issue number8
    Publication statusPublished - 2013

    Cite this