|
|
 Previous Article | Table of Contents | Next Article 
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.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
C. Johnson and M. J. Telen
Adhesion molecules and hydroxyurea in the pathophysiology of sickle cell disease
Haematologica,
April 1, 2008;
93(4):
481 - 485.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. A. Canalli, C. F. Franco-Penteado, S. T.O. Saad, N. Conran, and F. F. Costa
Increased adhesive properties of neutrophils in sickle cell disease may be reversed by pharmacological nitric oxide donation
Haematologica,
April 1, 2008;
93(4):
605 - 609.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. J. Telen
Role of Adhesion Molecules and Vascular Endothelium in the Pathogenesis of Sickle Cell Disease
Hematology,
January 1, 2007;
2007(1):
84 - 90.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Haynes Jr., B. Obiako, J. A. King, R. B. Hester, and S. Ofori-Acquah
Activated neutrophil-mediated sickle red blood cell adhesion to lung vascular endothelium: role of phosphatidylserine-exposed sickle red blood cells
Am J Physiol Heart Circ Physiol,
October 1, 2006;
291(4):
H1679 - H1685.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. G. Nolan, D. F. Wyszynski, L. A. Farrer, and M. H. Steinberg
Hemolysis-associated priapism in sickle cell disease
Blood,
November 1, 2005;
106(9):
3264 - 3267.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. D. Belcher, H. Mahaseth, T. E. Welch, A. E. Vilback, K. M. Sonbol, V. S. Kalambur, P. R. Bowlin, J. C. Bischof, R. P. Hebbel, and G. M. Vercellotti
Critical role of endothelial cell activation in hypoxia-induced vasoocclusion in transgenic sickle mice
Am J Physiol Heart Circ Physiol,
June 1, 2005;
288(6):
H2715 - H2725.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Goyal, S. T. Miller, M. R. Hammerschlag, M. Gelling, C. A. Gaydos, J. Hardick, B. J. Wood, T. Reznik, and S.P. Rao
Is Chlamydia pneumoniae Infection Associated With Stroke in Children With Sickle Cell Disease?
Pediatrics,
April 1, 2004;
113(4):
e318 - e321.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. D. Holtzclaw, D. Jack, S. M. Aguayo, J. R. Eckman, J. Roman, and L. L. Hsu
Enhanced Pulmonary and Systemic Response to Endotoxin in Transgenic Sickle Mice
Am. J. Respir. Crit. Care Med.,
March 15, 2004;
169(6):
687 - 695.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Perelman, S. K. Selvaraj, S. Batra, L. R. Luck, A. Erdreich-Epstein, T. D. Coates, V. K. Kalra, and P. Malik
Placenta growth factor activates monocytes and correlates with sickle cell disease severity
Blood,
August 15, 2003;
102(4):
1506 - 1514.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. D. Belcher, C. J. Bryant, J. Nguyen, P. R. Bowlin, M. C. Kielbik, J. C. Bischof, R. P. Hebbel, and G. M. Vercellotti
Transgenic sickle mice have vascular inflammation
Blood,
May 15, 2003;
101(10):
3953 - 3959.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. M. Matsui, A. Varki, and S. H. Embury
Heparin inhibits the flow adhesion of sickle red blood cells to P-selectin
Blood,
November 15, 2002;
100(10):
3790 - 3796.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. V. Graca-Souza, M. A. B. Arruda, M. S. de Freitas, C. Barja-Fidalgo, and P. L. Oliveira
Neutrophil activation by heme: implications for inflammatory processes
Blood,
May 13, 2002;
99(11):
4160 - 4165.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. DYUGOVSKAYA, P. LAVIE, and L. LAVIE
Increased Adhesion Molecules Expression and Production of Reactive Oxygen Species in Leukocytes of Sleep Apnea Patients
Am. J. Respir. Crit. Care Med.,
April 1, 2002;
165(7):
934 - 939.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Benkerrou, C. Delarche, L. Brahimi, M. Fay, E. Vilmer, J. Elion, M.-A. Gougerot-Pocidalo, and C. Elbim
Hydroxyurea corrects the dysregulated L-selectin expression and increased H2O2 production of polymorphonuclear neutrophils from patients with sickle cell anemia
Blood,
April 1, 2002;
99(7):
2297 - 2303.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Haynes Jr. and B. Obiako
Activated polymorphonuclear cells increase sickle red blood cell retention in lung: role of phospholipids
Am J Physiol Heart Circ Physiol,
January 1, 2002;
282(1):
H122 - H130.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. M. Matsui, L. Borsig, S. D. Rosen, M. Yaghmai, A. Varki, and S. H. Embury
P-selectin mediates the adhesion of sickle erythrocytes to the endothelium
Blood,
September 15, 2001;
98(6):
1955 - 1962.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. K. Adler, D. E. Salzman, M. H. Carabasi, W. P. Vaughan, V. V. B. Reddy, and J. T. Prchal
Fatal sickle cell crisis after granulocyte colony-stimulating factor administration
Blood,
May 15, 2001;
97(10):
3313 - 3314.
[Full Text]
[PDF]
|
|
|
|
|
|
|
K A Brown, S M Lewis, T A Hill, M G Macey, D A McCarthey, V A Grant, and D F Treacher
Leucodepletion and the interaction of polymorphonuclear cells with endothelium in systemic inflammatory response syndrome
Perfusion,
January 1, 2001;
16(1_suppl):
75 - 83.
[Abstract]
[PDF]
|
|
|
|
|
|
|
S. T. Miller, L. A. Sleeper, C. H. Pegelow, L. E. Enos, W. C. Wang, S. J. Weiner, D. L. Wethers, J. Smith, and T. R. Kinney
Prediction of Adverse Outcomes in Children with Sickle Cell Disease
N. Engl. J. Med.,
January 13, 2000;
342(2):
83 - 89.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. F. Rosse, M. Narla, L. D. Petz, and M. H. Steinberg
New Views of Sickle Cell Disease Pathophysiology and Treatment
Hematology,
January 1, 2000;
2000(1):
2 - 17.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
