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Am. J. Respir. Cell Mol. Biol., Volume 21, Number 4, October, 1999 528-536

Expression of Monocyte Chemotactic Protein (MCP)-1, MCP-2, and MCP-3 by Human Airway Smooth-Muscle Cells
Modulation by Corticosteroids and T-Helper 2 Cytokines

Jan L. Pype, Lieven J. Dupont, Patricia Menten, Els Van Coillie, Ghislain Opdenakker, Jo Van Damme, K. Fan Chung, Maurits G. Demedts, and Geert M. Verleden

Laboratory of Pneumology, Laboratory of Molecular Immunology, Rega Institute, Katholieke Universiteit, Leuven, Belgium; and Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom

We have demonstrated that, in addition to their contractile function, human airway smooth-muscle cells (HASMC) are able to express and to secrete chemokines of the monocyte chemotactic protein (MCP)/ eotaxin subfamily. This group of chemokines is believed to play a fundamental role in the development of allergic airway diseases such as asthma. The expression levels of MCP (MCP-1, -2, and -3) messenger RNA (mRNA) were compared with those of regulated on activation, normal T cells expressed and secreted (RANTES) mRNA in HASMC in culture. HASMC express MCP and RANTES mRNA after stimulation with interleukin (IL)-1beta , tumor necrosis factor-alpha , and interferon-gamma . MCP mRNA was maximal at 8 h, whereas RANTES mRNA expression was delayed to 24 h after stimulation. Further, significant differences were observed in the induction patterns of MCP and RANTES mRNA expression after stimulation with the individual cytokines. Dexamethasone (DEX) significantly inhibited cytokine-induced accumulation of MCP and RANTES mRNA, in contrast to IL-4, IL-10, and IL-13, which had no inhibitory effect on cytokine-induced chemokine expression. The cytokine-induced MCP mRNA expression in HASMC was associated with MCP release, which was inhibited by DEX and post-translationally by IL-4. HASMC can actively participate in the pathogenesis of asthma by the expression and release of chemokines, which are likely to play a critical role in the generation and regulation of the inflammatory response characteristic of allergic airway diseases.




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