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Articles in PresS, published online ahead of print January 25, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00279.2001
Submitted on July 24, 2001
Accepted on January 7, 2002
1 Pharmacology, University of Liverpool, Liverpool, Merseyside, United Kingdom
2 Medicine, Royal College of Surgeons in Ireland, Dublin, Dublin, Ireland
3 Medicine, Johns Hopkins University, Baltimore, MD, USA
In vivo, eosinophils localise to airway cholinergic nerves in antigen-challenged animals and inhibiting this localisation prevents antigen-induced hyperreactivity. In this study the mechanism of eosinophil localisation to nerves was investigated by examining adhesion molecule expression by cholinergic nerves. Immunohistochemical and functional studies demonstrated that primary cultures of parasympathetic nerves express vascular-cell adhesion molecule-1 (VCAM-1) and after cytokine pre-treatment with TNF-
and INF-
, intercellular-adhesion molecule-1 (ICAM-1). Eosinophils adhere to these parasympathetic neurones after cytokine pretreatment via a CD11/18 dependent pathway. Immunohistochemistry and Western blotting showed that a human cholinergic nerve cell line (IMR32) expressed VCAM-1 and ICAM-1. Inhibitory experiments using monoclonal blocking antibodies to ICAM-1, VCAM-1 or CD11/18 and with the VLA-4 peptide inhibitor, ZD7349 showed that eosinophils adhered to IMR32 cells via these adhesion molecules. The protein kinase C signalling pathway is involved in this process as a specific inhibitor attenuated adhesion. Eosinophil adhesion to IMR32 cells was associated with the release of eosinophil peroxidase and leukotriene C4. Thus, eosinophils adhere to cholinergic nerves via specific adhesion molecules and this leads to eosinophil activation and degranulation, this may be part of the mechanism of eosinophil-induced vagal hyperreactivity.
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