Details

Autor(en) / Beteiligte

• Curran, David R
• Morgan, Ross K
• Kingham, Paul J
• Durcan, Niamh
• McLean, W. Graham
• Walsh, Marie Therese
• Costello, Richard W

Titel

Mechanism of eosinophil induced signaling in cholinergic IMR-32 cells

Ist Teil von

• American journal of physiology. Lung cellular and molecular physiology, 2005-02, Vol.288 (2), p.L326-L332

Ort / Verlag

United States

Erscheinungsjahr

2005

Link zum Volltext

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 1 Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland; and 2 Department of Pharmacology and Therapeutics, University of Liverpool, Liverpool, United Kingdom Submitted 6 July 2004 ; accepted in final form 30 September 2004 Eosinophils interact with nerve cells, leading to changes in neurotransmitter release, altered nerve growth, and protection from cytokine-induced apoptosis. In part, these interactions occur as a result of activation of neural nuclear factor (NF)- B, which is activated by adhesion of eosinophils to neural intercellular adhesion molecule-1 (ICAM-1). The mechanism and consequence of signaling after eosinophil adhesion to nerve cells were investigated. Eosinophil membranes, which contain eosinophil adhesion molecules but not other eosinophil products, were coincubated with IMR-32 cholinergic nerve cells. The studies showed that there were two mechanisms of activation of NF- B, one of which was dependent on reactive oxygen species, since it was inhibited with diphenyleneiodonium. This occurred at least 30 min after coculture of eosinophils and nerves. An earlier phase of NF- B activation occurred within 2 min of eosinophil adhesion and was mediated by tyrosine kinase-dependent phosphorylation of interleukin-1 receptor-associated kinase-1 (IRAK-1). Coimmunoprecipitation experiments showed that both extracellular signal-regulated kinase 1/2 and IRAK-1 were recruited to ICAM-1 rapidly after coculture with eosinophil membranes. This was accompanied by an induction of ICAM-1, which was mediated by an IRAK-1-dependent pathway. These data indicate that adhesion of eosinophils to IMR-32 nerves via ICAM-1 leads to important signaling events, mediated via IRAK-1, and these in turn lead to expression of adhesion molecules. plasticity; cholinergic; neural; adhesion Address for reprint requests and other correspondence: Richard W. Costello, Dept. of Medicine, RCSI, Beaumont Hospital, Dublin 9, Ireland (E-mail: rcostello{at}rcsi.ie )