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Published ahead of print on July 10, 2003, doi:10.1165/rcmb.2003-0188OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 3, March 2004, 333-341

A more recent version of this article appeared on March 1, 2004
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Submitted on May 9, 2003
Revised on July 8, 2003

Effect of eosinophil adhesion on intracellular signalling in cholinergic nerve cells

Marie-Therese Walsh1, David R Curran1, Paul J Kingham2, Ross K Morgan1, Niamh Durcan1, Gerald J Gleich3, W. Graham McLean2, and Richard W Costello1*

1 Medicine, Beaumont Hospital, Dublin, Dublin, Ireland, 2 Pharmacology and Therapeutics, University of Liverpool, Liverpool, United Kingdom, 3 Dermatology, University of Utah, Utah, UT, USA

* To whom correspondence should be addressed. E-mail: rcostello{at}rcsi.ie.

Eosinophil localisation to cholinergic nerves occurs in a variety of inflammatory conditions including asthma. This localisation is mediated by interactions between eosinophil integrins and neuronal vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Eosinophil-nerve cell interactions lead to generation of neuronal reactive oxygen species and release of eosinophil proteins. The effects of eosinophil adhesion on neuronal intracellular signalling pathways were investigated. Eosinophil adhesion to IMR32 cholinergic nerves led to a rapid and sustained activation of the nuclear transcription factors NF-{kappa}B and AP-1 in the nerve cells. Eosinophil binding to neuronal ICAM-1 led to a rapid activation of ERK1/2 in nerve cells . Inhibition of ERK1/2 prevented NF-{kappa}B activation. Eosinophil adhesion to VCAM-1 resulted in AP-1 activation, mediated partially by rapid activation of the p38 MAP kinase. These data show that adhesion of eosinophils induced MAP kinase-dependent activation of the transcription factors NF-{kappa}B and AP-1 in nerve cells, indicating that eosinophil adhesion may control nerve growth and phenotype.




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