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Blood Polymorphonuclear Leukocytes From the Majority of Sickle Cell
Patients in the Crisis Phase of the Disease Show Enhanced Adhesion to
Vascular Endothelium and Increased Expression of CD64
Emma Fadlon,
Susanne Vordermeier,
Thomas C. Pearson,
Anthony R. Mire-Sluis,
Dudley C. Dumonde,
Julia Phillips,
Keith Fishlock, and
K. Alun Brown
From the Departments of Immunology and Haematology, St Thomas'
Hospital, London; and the Department of Immunology, National Institute
for Biological Standards and Control, South Mimms, Hertfordshire, UK.
There is increasing interest in the role of blood polymorphonuclear
leukocytes (PMNs) in the pathogenesis of sickle cell crisis. We studied
the adherence of PMNs from 18 sickle cell patients in crisis, 25 out of
crisis, and 43 healthy subjects (controls) to monolayers of human
umbilical cord endothelium that were either untreated or pretreated
with tumor necrosis factor  (TNF). Overall, the PMNs from
patients in crisis were more adherent than control PMNs to untreated
endothelial monolayers (mean 53% increase; P < .001) and
TNF-treated monolayers (mean 41% increase; P < .002). Increased adhesiveness was not associated with an abnormal expression of CD11a, CD11b, CD11c, CD18, CD62L, or CD15. There was an increase in
the number of PMNs expressing CD64 in patients in crisis (median value,
44%) compared with patients out of crisis (median, 21%; P = .025) and controls (median, 6.5%; P < .001). Sera from
patients in crisis had normal levels of granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor,
interferon- , TNF, interleukin-1 (IL-1), IL-6, or IL-8 and did not
modify the adherence of PMNs or their expression of CD64. Only IFN-
induced CD64 expression on PMNs, but this effect was not associated
with enhanced binding to endothelium. Because PMNs bound to endothelial monolayers were CD64+ and CD64-enriched PMNs were 7 times
more adherent to endothelial monolayers than CD64-depleted PMNs, it is
likely that CD64 is a marker of adherent PMNs. Two of the three
anti-CD64 antibodies used in our antibody blocking studies (clones 32.2 and 197) partially inhibited the binding of sickle cell PMNs to
untreated endothelium (mean inhibitions of 33% [P = .01]
and 21% [P = .03], respectively), whereas
only one (clone 197) inhibited binding to TNF-treated endothelium
(mean inhibition, 29%; P = .004). In some patients with
sickle cell disease, an enhanced PMN adhesion to vascular endothelium
could contribute to the vascular occlusion that characterizes the acute
crisis of the disease.
Blood, Vol. 91 No. 1 (January 1), 1998:
pp. 266-274
© 1998 by The American Society of Hematology.
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