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Expression of P-Selectin on Hepatic Endothelia and Platelets
Promoting Neutrophil Removal by Liver Macrophages
Jialan Shi,
Yoshihiro Kokubo, and
Kenjiro Wake
From the Department of Anatomy, School of Medicine, Tokyo Medical and
Dental University, Tokyo 113, Japan.
The role of P-selectin on polymorphonuclear leukocyte
(PMN) adhesion-induced PMN elimination in the liver is
unclear. Our objectives were to show the expression and distribution of
P-selectin in rat liver, as well as to evaluate the changes in the
modulation of the expression of P-selectin and its role in the
accumulation and sequestration of PMNs. The intravenous administration
of endotoxin markedly increased the expression of P-selectin on the
venous and sinusoidal endothelial cells, as well as on the platelets trapped in the liver. Its expression peaked at 6 hours postinjection and was associated with a rapid increase in the aggregation and elimination of PMNs in the hepatic sinusoids. Combined treatment with
an antibody to P-selectin or with low molecular weight heparin, a
P-selectin antagonist, blocked the P-selectin, significantly reduced
the arrest of PMNs, and delayed their removal in the liver. Pretreatment with gadolinium chloride inhibited phagocytosis of PMNs by
the Kupffer cells, decreased the expression of P-selectin, and limited
the hepatic accumulation of PMNs. Thus, P-selectin played a role in
accumulation and elimination of PMNs from the liver. Results also
suggest that activated Kupffer cells can modulate the expression of
P-selectin in the liver and influence the homeostasis of PMNs in the
circulation during acute inflammation.
Blood, Vol. 92 No. 2 (July 15), 1998:
pp. 520-528
© 1998 by the American Society of Hematology.
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