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Chronic expression of P-selectin on endothelial cells stimulated by the
T-cell cytokine, interleukin-3
Y Khew-Goodall, CM Butcher, MS Litwin, S Newlands, EI Korpelainen, LM Noack, MC Berndt, AF Lopez, JR Gamble and MA Vadas
Hanson Centre for Cancer Research, Institute of Medical and Veterinary
Science, Adelaide, Australia.
P-selectin expressed on the surface of endothelium mediates leukocyte
adhesion in vitro and rolling in vivo. Several inducers of cell-surface
P-selectin expression on endothelial cells (EC) have previously been
identified, all of which yield transient cell-surface expression of P-
selectin lasting minutes to a few hours. We now show that a T- lymphocyte
product, interleukin-3 (IL-3), stimulates the long-term endothelial cells
(HUVEC). IL-3 induced cell-surface P-selectin expression in two phases. An
initial peak at 10 minutes was followed by a prolonged upregulation
beginning 16 hours after IL-3 addition and lasting at least 4 days. The
level of P-selectin expression induced by IL-3 added for 48 hours was
similar to that induced by treatment of HUVEC for 10 minutes with thrombin,
and the effect of adding IL-3 for 48 hours followed by thrombin for 10
minutes was additive. Induction of cell-surface P-selectin expression by
IL-3 was blocked by pretreatment of EC with a blocking monoclonal antibody
against the IL-3 receptor alpha-chain. Lipopolysaccharide (LPS), tumor
necrosis factor alpha (TNF alpha) and a mutant form of IL-3 with decreased
potency did not induce cell-surface P-selectin expression after 48 hours'
incubation with HUVEC, suggesting that the effect was specific to IL-3. The
increase in cell-surface P-selectin expression occurring after 16 hours of
incubation with IL-3 was accompanied by a similar prolonged increase in the
steady-state mRNA level that was not observed at 10 minutes after IL-3
addition. As T-lymphocyte infiltration is a hallmark of chronic
inflammation, our observations suggest that the secretion of IL-3 by T
lymphocytes may serve to maintain the inflammatory state during chronic
inflammation.
Volume 87,
Issue 4,
pp. 1432-1438,
02/15/1996
Copyright © 1996 by The American Society of Hematology
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