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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.00278.2001
Submitted on July 24, 2001
Accepted on January 7, 2002
1 Department of Pharmacology and Therapeutics, University of Liverpool, Liverpool, L69 3GE, United Kingdom
2 Medicine, Royal College of Surgeons in Ireland, Dublin, Dublin9, Ireland
Eosinophils adhere to airway cholinergic nerves and influence nerve cell function by releasing granule proteins onto inhibitory neuronal M2 muscarinic receptors. This study investigated the mechanism of eosinophil degranulation by cholinergic nerves. Eosinophils were co-cultured with IMR32 cholinergic nerve cells and eosinophil peroxidase (EPO) or leukotriene C4 (LTC4) release were measured. Co-culture of eosinophils with nerves significantly increased EPO and LTC4 release compared with eosinophils alone. IMR32 cells, like parasympathetic nerves, express the adhesion molecules vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Inhibition of these adhesion molecules alone or in combination significantly inhibited the eosinophil degranulation. IMR32 cells also significantly augmented the eosinophil degranulation produced by formyl-met-leu-phe (fMLP). Eosinophil adhesion to IMR32 cells resulted in an ICAM-1-mediated production of reactive oxygen species (ROS) via a neuronal NADPH oxidase, inhibition of which significantly inhibited eosinophil degranulation. Additionally, eosinophil adhesion increased the release of acetylcholine from IMR32 cells. These neuro-inflammatory cell interactions may be relevant in a variety of inflammatory and neurological conditions.
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