Cd18 integrin and intercellular adhesion molecule-1 (cd54)
dependent neutrophil.
Nagendra, Attibele R., Judith K. Mickelson, and C. Wayne Smith.
Speros P. Martel Laboratory of Leukocyte Biology, Department of
Pediatrics, and Section of Cardiology, Department of Medicine, Baylor
College of Medicine, Houston, Texas
APStracts 3:0158G, 1996.
We investigated the hypothesis that CD54 (intercellular adhesion
molecule-1, ICAM-1) expressed on hepatocytes will support [beta]2
(CD18) integrin-dependent adhesion of neutrophils. An in vitro model
using C3A cells (a human hepatoblastoma cell line exhibiting many
characteristics of normal hepatocytes) and human neutrophils was
utilized. C3A cells were stimulated with IL-1[beta], TNF[alpha], or
IFN[delta] for 24 hours to induce expression of CD54, and adhesion of
neutrophils was found to be markedly increased. Detailed studies with
IFN[delta]-stimulated (100 U/ml) C3A cells revealed that this
adhesion involved CD11a/CD18 (LFA-1) and CD54, and was dependent on
low levels of IL-8 produced by the stimulated hepatocytes. Addition
of higher concentrations of chemotactic factor (e.g., IL-8) further
augmented adhesion and recruited contributions of CD11b/CD18 (Mac-1).
In contrast to LFA-1, Mac-1 appeared to recognize a CD54-independent
ligand constitutively expressed on the hepatocytes. Such close
apposition of neutrophils to hepatocytes may increase the potential
for parenchymal cell injury by providing a short distance through
which cytotoxic factors such as reactive oxygen or proteolytic
enzymes could act.
Received 25 April 1996; accepted in final form 8 August 1996.
APS Manuscript Number G159-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996