期刊
BLOOD
卷 117, 期 20, 页码 5503-5513出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-09-309161
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资金
- Swedish Research Council [K2010-65X-14008]
- Torsten and Ragnar Soderberg Foundation
- Fund for Renal Research
- Crown Princess Lovisa's Society for Child Care
- Konung Gustaf V's 80-arsfond
- Fanny Ekdahl's Foundation
- Queen Silvia Jubilee Fond
- Royal Swedish Academy of Sciences
Hemolytic uremic syndrome (HUS) is commonly associated with Shiga toxin (Stx)-producing Escherichia coli O157:H7 infection. This study examined patient samples for complement activation on leukocyte-platelet complexes and microparticles, as well as donor samples for Stx and lipopolysaccharide (O157LPS)-induced complement activation on platelet-leukocyte complexes and microparticles. Results, analyzed by flow cytometry, showed that whole blood from a child with HUS had surface-bound C3 on 30% of platelet-monocyte complexes compared with 14% after recovery and 12% in pediatric controls. Plasma samples from 12 HUS patients were analyzed for the presence of microparticles derived from platelets, monocytes, and neutrophils. Acute-phase samples exhibited high levels of platelet microparticles and, to a lesser extent, monocyte microparticles, both bearing C3 and C9. Levels decreased significantly at recovery. Stx or O157LPS incubated with donor whole blood increased the population of platelet-monocyte and platelet-neutrophil complexes with surface-bound C3 and C9, an effect enhanced by costimulation with Stx and O157LPS. Both Stx and O157LPS induced the release of C3- and C9-bearing microparticles from platelets and monocytes. Released microparticles were phagocytosed by neutrophils. The presence of complement on platelet-leukocyte complexes and microparticles derived from these cells suggests a role in the inflammatory and thrombogenic events that occur during HUS. (Blood. 2011;117(20):5503-5513)
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