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N-acetylcysteine reduces chemokine release via inhibition of p38 MAPK in human airway smooth muscle cells

KU Leuven, Laboratory of Pneumology, Leuven, Belgium

CORRESPONDENCE: G.M. Verleden, University Hospital Gasthuisberg, Dept of Respiratory Disease, 49 Herestraat, Leuven B-3000, Belgium. Fax: 32 16346803. E-mail: geert.verleden@uz.kuleuven.ac.be

Keywords: human airway smooth muscle cells, interleukin-1ß, N-acetylcysteine, oxidative stress, p38 mitogen-activated protein kinase, signal transduction

Received: July 18, 2002
Accepted February 28, 2003

W.A. Wuyts is a research fellow of the "Fonds voor wetenschappelijk onderzoek Vlaanderen". The work was funded by the Fonds voor wetenschappelijk onderzoek Vlaanderen (project no. G 0220.99). G.M. Verleden is holder of the Glaxo-SmithKline Chair for Respiratory Pharmacology at the Katholieke Universiteit Leuven, Belgium.

Reactive oxygen species are involved in the activation of several mitogen-activated protein kinases (MAPKs), key-players in the production of several cytokines. Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1ß-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).

NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46±11% (n=7) and 87±4% (n=6), respectively; the eotaxin release was inhibited by 75±5% (n=7), whereas the MCP-1 release was decreased by 69±4% (n=10). NAC (1 mM) also decreased the IL-1ß-induced activation of p38 MAPK.

Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1ß-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39±12% with 1 mM NAC.

The present study demonstrated that N-acetylcysteine inhibits the interleukin-1ß-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase. This study has also shown that N-acetylcysteine decreases the interleukin-1ß-induced production of reactive oxygen species, as suggested by a reduction in the 8-isoprostane production.

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