Melatonin suppresses acrolein-induced IL-8 production in human pulmonary fibroblasts
Article first published online: 23 SEP 2011
© 2011 John Wiley & Sons A/S
Journal of Pineal Research
Volume 52, Issue 3, pages 356–364, April 2012
How to Cite
Kim, G.-D., Lee, S. E., Kim, T.-H., Jin, Y.-H., Park, Y. S. and Park, C.-S. (2012), Melatonin suppresses acrolein-induced IL-8 production in human pulmonary fibroblasts. Journal of Pineal Research, 52: 356–364. doi: 10.1111/j.1600-079X.2011.00950.x
- Issue published online: 20 MAR 2012
- Article first published online: 23 SEP 2011
- Accepted manuscript online: 22 AUG 2011 03:50PM EST
- Received July 14, 2011; Accepted August 18, 2011.
Abstract: Cigarette smoke (CS) causes harmful alterations in the lungs and airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). In addition to COPD, active cigarette smoking causes other respiratory diseases and diminishes health status. Furthermore, recent studies show that, α, β-unsaturated aldehyde acrolein in CS induces the production of interleukin (IL)-8, which is known to be related to bronchitis, rhinitis, pulmonary fibrosis, and asthma. In addition, lung and pulmonary fibroblasts secrete IL-8, which has a chemotactic effect on leukocytes, and which in turn, play a critical role in lung inflammation. On the other hand, melatonin regulates circadian rhythm homeostasis in humans and has many other effects, which include antioxidant and anti-inflammatory effects, as demonstrated by the reduced expressions of iNOS, IL-1β, and IL-6 and increased glutathione (GSH) and superoxide dismutase activities. In this study, we investigated whether melatonin suppresses acrolein-induced IL-8 secretion in human pulmonary fibroblasts (HPFs). It was found that acrolein-induced IL-8 production was accompanied by increased levels of phosphorylation of Akt and extracellular signal-regulated kinases (ERK1/2) in HPFs, and that melatonin suppressed IL-8 production in HPFs. These results suggest that melatonin suppresses acrolein-induced IL-8 production via ERK1/2 and phosphatidylinositol 3-kinase (PI3K)/Akt signal inhibition in HPFs.