1. Nucleation of platelets with blood-borne pathogens on Kupffer cells precedes other innate immunity and contributes to bacterial clearance.
- Author
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Wong CH, Jenne CN, Petri B, Chrobok NL, and Kubes P
- Subjects
- Animals, Blood Platelets immunology, Immunity, Innate immunology, Kupffer Cells immunology, Liver cytology, Liver immunology, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Confocal, Platelet Adhesiveness immunology, Specific Pathogen-Free Organisms, Bacillus cereus immunology, Blood Platelets microbiology, Kupffer Cells microbiology, Liver microbiology, Methicillin-Resistant Staphylococcus aureus immunology, Platelet Activation immunology, Platelet Glycoprotein GPIIb-IIIa Complex immunology
- Abstract
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 GPIbα-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.
- Published
- 2013
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