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Mediators of Inflammation
Volume 10 (2001), Issue 3, Pages 135-142

Pro-inflammatory cytokines induce c-fos expression followed by IL-6 release in human airway smooth muscle cells

1Department of Pharmacology, Erasmus University Medical Center (EMCR), Dr. Molewaterplein 50, 3015 GE, The Netherlands
2Department of Paediatrics-Respiratory Medicine, Sophia Children's Hospital, Rotterdam, The Netherlands
3Department of Pulmonary-Medicine, Erasmus University Medical Centre Rotterdam, The Netherlands

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background: Airway smooth muscle (ASM) is considered to be a target for mediators released during airway inflammation.

Aims: To investigate the expression of c-fos, a constituent of the transcription factor activator protein-1, in human ASM cells. In addition, to measure the release of interleukin (IL)-6 into the conditioned medium of stimulated ASM cells, as well as DNA biosynthesis and changes in cell number.

Methods: Serum-deprived human ASM cells in the G0/G1 phase were stimulated with the pro-inflammatory cytokines; tumour necrosis factor-α, IL-1β, IL-5 and IL-6. The expression of mRNA encoding the proto-oncogene c-fos was measured by Northern blot analysis. Cell proliferation was assessed by {3H}-thymidine incorporation assays and cell counting, and IL-6 levels in cell-conditioned medium were measured by enzyme-linked immunosorbent assay.

Results: All of the cytokines investigated induced a rapid (within 1h) and transient increase in the expression of mRNA encoding c-fos, followed by the expression and enhanced release of IL-6. Cell proliferation remained unchanged in cytokine-stimulated cells.

Conclusions: Cytokine-induced c-fos expression in human ASM cells could be described as a marker of cell ‘activation'. The possible association of these results with airway inflammation, through secondary intracellular mechanisms such as cytokine production, is discussed.