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

被引：290

作者：

Wong, Connie H. Y. ^{[1
]}

Jenne, Craig N. ^{[2
]}

Petri, Bjoern ^{[1
]}

Chrobok, Navina L. ^{[1
]}

Kubes, Paul ^{[1
,2
]}

机构：

[1] Univ Calgary, Dept Physiol & Pharmacol, Calvin Phoebe & Joan Snyder Inst Chron Dis, Calgary, AB T2N 1N4, Canada

[2] Univ Calgary, Dept Crit Care Med, Calvin Phoebe & Joan Snyder Translat Lab Crit Car, Calgary, AB T2N 1N4, Canada

来源：

NATURE IMMUNOLOGY | 2013年 / 14卷 / 08期

基金：

加拿大健康研究院;

关键词：

NEUTROPHIL EXTRACELLULAR TRAPS; BACILLUS-ANTHRACIS SPORES; APOPTOSIS; SPLEEN; COAGULATION; EXPRESSION; CLODRONATE; SURVIVAL; ADHESION; LIVER;

D O I：

10.1038/ni.2631

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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 GPIb alpha-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.

引用

页码：785 / +

页数：10

共 47 条

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