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Blood, 15 January 2001, Vol. 97, No. 2, pp. 465-472
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Interleukin 11 significantly increases plasma von Willebrand
factor and factor VIII in wild type and von Willebrand disease mouse
models
Cécile V. Denis,
Kyubum Kwack,
Simin Saffaripour,
Srinivas Maganti,
Patrick André,
Robert G. Schaub, and
Denisa D. Wagner
From The Center for Blood Research and the Department
of Pathology, Harvard Medical School, Boston, MA, and Wyeth/Genetics
Institute, Cambridge, MA.
Interleukin (IL)-11 is a cytokine with thrombopoietic activity that
has been shown to increase plasma von Willebrand factor (vWf) in
preliminary clinical studies. This led to further evaluation of
the effect of recombinant human (rh)IL-11 on vWf and factor VIII
(FVIII) secretion. In vitro, rhIL-11 did not increase vWf production by
cultured endothelial cells, which suggests an indirect mechanism. Also,
in vivo, plasma vWf was not elevated in mice shortly after a single
intravenous (IV) bolus injection of 250 or 1000 µg/kg rhIL-11. The
effect of continuous exposure to rhIL-11 was accessed by treating wild
type mice for 7 consecutive days with subcutaneous 250 µg/kg/d
rhIL-11. Platelet counts increased by 25% and 40% after 4 and 7 days,
respectively. Plasma vWf and FVIII levels increased 2-fold after 4 and
7 days. Surprisingly, no effect of rhIL-11 on vWf or FVIII messenger
RNA was observed, which suggests that the regulation by rhIL-11
occurs after transcription. No increase in soluble P-selectin
was observed after rhIL-11 treatment, indicating that platelet
activation is not the source of elevated vWf. Similarly to wild type
mice, vWf heterozygous mice responded to rhIL-11 treatment by a
significant increase in platelet counts and vWf and FVIII levels.
Importantly, in vWf-deficient mice, rhIL-11 also induced a significant
increase in FVIII independent of vWf and was able to reduce skin
bleeding time. These results suggest that a clinical evaluation of the
effects of rhIL-11-induced vWf/FVIII elevation in maintaining
hemostasis in mild hemophilia A or von Willebrand disease would be worthwhile.
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