Stimulation of both human bronchial epithelium and neutrophils is
necessary for maximal interactive adhesion.
Bloemen, P. G. M., M. C. Van Den Tweel, P. A. J. Henricks, F. Engels,
M. J. Van De Velde, F. J. Blomjous, and F. P. Nijkamp.
Department of Pharmacology, Utrecht Institute for Pharmaceutical
Sciences, Utrecht University, PO Box 80.082, 3508 TB Utrecht, and
Department of Pathology, St. Antonius Hospital Nieuwegein, The
Netherland
APStracts 2:0163L, 1995.
It has become clear that the bronchial epithelium is not just a
passive barrier, but plays an active role in inflammation. It can
produce several inflammatory mediators and does express cell adhesion
molecules of which ICAM-1 can be upregulated by cytokines like IFN-_.
In the present study, we analyzed in detail the interaction of
neutrophils with human bronchial epithelial cells, both primary
cultured cells (HBEC) and the bronchial epithelial cell line BEAS-2B.
Confluent monolayers of epithelial cells were incubated with freshly
isolated 51cromium-labeled neutrophils for 30 min at 37 degrees C
whereafter the non-adherent cells were removed by washing gently.
Stimulation of the epithelial cells with IFN-_ or the combination of
IFN-_ and TNF-[alpha] (which doubles the ICAM-1 expression),
increased neutrophil adhesion. Activation of the neutrophils
themselves with fMLP, PAF, or TNF-[alpha] also caused a profound
enhancement of the adhesion. A significant additional increase was
found when the epithelial cells had been exposed to IFN-_ and the
neutrophils were stimulated with fMLP simultaneously. This effect was
even more pronounced with epithelium preincubated with IFN-_ and TNF
-[alpha]. Using monoclonal antibodies against CD18 and ICAM-1, it was
demonstrated that the increased adhesion was mainly mediated by the
ICAM-1/[beta]2 integrin interaction. This study highlights that both
the activation state of the bronchial epithelial cells and the
activation state of the neutrophils are critical for their
interactive adhesion.
Received 1 February 1995; accepted in final form 2 August 1995.
APS Manuscript Number L31-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.