This article corrects:

  1. Wednesday, 27 July 2011 Volume 9, Issue s2, 499–711, Article first published online: 31 July 2011

In [1], the abstract was published incorrectly, therefore, it is now reproduced in full below:


EspP, an extracellular serine protease from enterohemorrhagic Escherichia coli, induces coagulopathy in human plasma and fibrinolysis in whole blood

S. KHAN*, K. H. M. KUO†, E. BRNJAC‡, M. L. RAND§, E. F. PAI¶ and A. E. CHESNEY**

* Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada; †Department of Medical Oncology and Hematology, University Health Network; ‡Department of Clinical Pathology, Sunnybrook Health Sciences Centre; §Division of Hematology, The Hospital for Sick Children; ¶Departments of Biochemistry, Molecular Genetics and Medical Biophysics, University of Toronto, and Division of Cancer Genomics and Proteomics, Ontario Cancer Institute, University Health Network; and **Department of Clinical Pathology, Sunnybrook Health Sciences Centre, Toronto, ON, Canada

Summary.  EspP (E. coli secreted serine protease) is a virulence factor in diarrhea-associated Hemolytic Uremic Syndrome. It cleaves human factor V in vitro (Brunder et al., Mol Microbiol 1997, 24: 767–78) and we have observed that EspP also cleaves factor VIII. Here, we further investigate the effects of EspP on hemostasis. Incubation of citrated whole blood (= 5 donors) with 1 mg mL−1 EspP at 37°C for 4 h prolonged the PT by 32.7 s (95% CI 26.7–38.8, = 0.0001), aPTT by 77.5 s (95% CI 56.4–98.6, = 0.0005) and TT by 10.2 s (95% CI 9.2–11.1, < 0.0001). Factor V activity decreased by 0.66 U mL−1 (95% CI 0.54–0.78, = 0.0001), factor VII by 0.74 U mL−1 (95% CI 0.40–1.07, = 0.004), factor VIII by 0.58 U mL−1 (95% CI 0.37–0.80, = 0.002) and factor XII by 0.46 U mL−1 (95% CI 0.27–0.65, = 0.005). Prothrombin activity decreased by 0.17 U mL−1 (95% CI 0.09–0.25, = 0.007) but remained above 0.70 U mL−1. Factors IX, X and XI activities were unchanged. Interestingly, when analyzed by whole blood thrombelastography (= 4 donors), reaction time (R) decreased by 7.0 min (95% CI 3.7–10.3, = 0.007), clot formation time (K) decreased by 0.86 min (95% CI 0.22–1.50, = 0.023), and clot kinetics (alpha angle) increased by 9.5 (95% CI 8.3–10.8, = 0.0002), suggesting an accelerated rate of platelet-fibrin clot formation. Moreover, maximum amplitude of clot (MA) and percent clot lysis (LY30) were indicative of enhanced fibrinolysis; MA decreased, and LY30 increased, by 25.9 mm (95% CI 11.0–40.8, = 0.012), and 27.1% (95% CI 17.5–71.7, = 0.15), respectively, when samples were incubated with EspP for 4 h, but by 21.9 mm (95% CI 10.8–31.3, = 0.009), and 40.5% (95% CI 18.6–62.3, = 0.010), respectively, when samples were incubated with EspP for only 2 h. Our results show that EspP alters hemostasis in vitro by decreasing the activities of factors V, VII, VIII and XII, by enhancing platelet-fibrin clot formation, and by accelerating fibrinolysis. Further work is required to delineate the mechanisms involved.