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Blood, Vol. 95 No. 10 (May 15), 2000:
pp. 3146-3152
Interleukin-13 induces PSGL-1/P-selectin-dependent adhesion of
eosinophils, but not neutrophils, to human umbilical vein
endothelial cells under flow
Gerrit Woltmann,
Claire A. McNulty,
Grant Dewson,
Fiona A. Symon, and
Andrew J. Wardlaw
From the Division of Respiratory Medicine, University of Leicester
School of Medicine, Glenfield Hospital, Leicester, UK.
Selective eosinophil accumulation is a hallmark of diseases such as
asthma. In a model of chronic eosinophilic inflammation, we have
previously shown that the tethering step in eosinophil adhesion is
mediated by PSGL-1 binding to P-selectin. The Th2-associated cytokine
IL-13 is of potential importance in allergic disease. We have therefore
investigated whether IL-13 can mediate eosinophil binding to human
umbilical vein endothelial cells (HUVEC) through P-selectin. IL-13
caused dose- and time-dependent increases of P-selectin expression, as
assessed by flow and laser scanning cytometry. A similar degree of
expression was observed with IL-4. There was no effect on E-selectin or
ICAM-1 expression. Tumor necrosis factor- induced the
expression of VCAM-1, E-selectin, and ICAM-1 but had no effect on
P-selectin expression. IL-13 increased the production of mRNA for
surface and soluble variants of P-selectin. Under flow conditions,
eosinophils, but not neutrophils, showed enhanced binding to
IL-13 and to IL-4-stimulated HUVEC compared to
medium-cultured cells. Eosinophil adhesion was completely inhibited by
a blocking monoclonal antibody against PSGL-1 and P-selectin. Anti-VLA-4 and anti-VCAM-1 antibodies inhibited binding to a lesser extent. Thus, at physiologic levels of expression induced by Th2 cytokines, P-selectin/PSGL-1 supported eosinophil but not neutrophil adhesion. This mechanism is likely to be a key event leading to the
selective accumulation of eosinophils in allergic inflammation.
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