|
|
Previous Article | Table of Contents | Next Article 
Relation of the CD11/CD18 family of leukocyte antigens to the transient
neutropenia caused by chemoattractants
C Lundberg and SD Wright
Department of Inflammation Research, Pharmacia AB, Uppsala, Sweden.
Adherence of leukocytes to the endothelium is a prerequisite for
infiltration and accumulation of cells at an inflammatory site. Recent
studies suggest that the CD11/CD18 family of adhesion-promoting receptors
plays a crucial role in the initial adherence of polymorphonuclear
leukocytes (PMNs) to endothelium. We have studied the effect of the
anti-CD18 monoclonal antibody (MoAb) IB4, on movement of PMN in rabbits.
Accumulation of PMNs in the skin induced by a local injection of the
chemoattractant, zymosan-activated serum (ZAS), was strongly inhibited, in
a dose-dependent fashion, by intravenous injection of IB4. A greater than
95% reduction in PMN accumulation was seen with 1 mg IB4/kg body weight,
the highest dose used. PMN-dependent plasma leakage in the ZAS-injected
skin sites was also inhibited by pretreatment with MoAb IB4, with a similar
dose dependence. Histamine- induced plasma leakage, which is PMN
independent, was not affected by this treatment. F(ab)2 fragments of IB4
were as effective as the whole immunoglobulin G molecule in reducing PMN
accumulation. The half-life of circulating IB4 in rabbits was found to be
11.5 hours. These results are consistent with in vitro studies that show
that binding of PMNs to endothelium requires both expression of CD11/CD18
molecules and activation of the PMNs by agonists, and confirm that sites on
CD11/CD18 that recognize endothelial cells are blocked by IB4. Other
investigators have shown that injection of chemoattractants into the blood
stream causes a rapid neutropenia associated with accumulation of PMNs in
the lung. We find that intravenous treatment of animals with IB4 did not
block the transient accumulation of PMNs in the lung induced by
formyl-methionyl-leucyl-phenylalanine, suggesting that this accumulation
occurs by a mechanism that does not require CD11/CD18 molecules.
Volume 76,
Issue 6,
pp. 1240-1245,
09/15/1990
Copyright © 1990 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:

|
 |

|
 |
 
A. R. Burns, C. W. Smith, and D. C. Walker
Unique Structural Features That Influence Neutrophil Emigration Into the Lung
Physiol Rev,
April 1, 2003;
83(2):
309 - 336.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. GARDINALI, E. BORRELLI, O. CHIARA, C. LUNDBERG, P. PADALINO, L. CONCIATO, C. CAFARO, S. LAZZI, P. LUZI, P. P. GIOMARELLI, et al.
Inhibition of CD11-CD18 Complex Prevents Acute Lung Injury and Reduces Mortality after Peritonitis in Rabbits
Am. J. Respir. Crit. Care Med.,
March 1, 2000;
161(3):
1022 - 1029.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. C. Barnett Jr., E. E. Moore, G. W. Mierau, D. A. Partrick, W. L. Biffl, D. J. Elzi, and C. C. Silliman
ICAM-1-CD18 interaction mediates neutrophil cytotoxicity through protease release
Am J Physiol Cell Physiol,
June 1, 1998;
274(6):
C1634 - C1644.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
K. Tanji-Matsuba, S. F. van Eeden, Y. Saito, M. Okazawa, M. E. Klut, S. Hayashi, and J. C. Hogg
Functional Changes in Aging Polymorphonuclear Leukocytes
Circulation,
January 13, 1998;
97(1):
91 - 98.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|
|