Funding sources None.
Smoking and pathogenesis of psoriasis: a review of oxidative, inflammatory and genetic mechanisms
Article first published online: 2 NOV 2011
© 2011 The Authors. BJD © 2011 British Association of Dermatologists 2011
British Journal of Dermatology
Volume 165, Issue 6, pages 1162–1168, December 2011
How to Cite
Armstrong, A.W., Armstrong, E.J., Fuller, E.N., Sockolov, M.E. and Voyles, S.V. (2011), Smoking and pathogenesis of psoriasis: a review of oxidative, inflammatory and genetic mechanisms. British Journal of Dermatology, 165: 1162–1168. doi: 10.1111/j.1365-2133.2011.10526.x
Conflicts of interest None declared.
- Issue published online: 24 NOV 2011
- Article first published online: 2 NOV 2011
- Accepted manuscript online: 20 JUL 2011 10:54AM EST
- Accepted for publication 4 July 2011
Recent studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Smoking initiates formation of free radicals that stimulate cell signalling pathways active in psoriasis including mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB) and Janus kinase/signal transducers and activators of transcription (JAK-STAT). Smoking damages the skin by increasing formation of reactive oxygen species and decreasing the gene expression of antioxidants. Nicotine also stimulates innate immune cells integral to the pathogenesis of psoriasis including dendritic cells, macrophages and keratinocytes. These cells release cytokines that activate T lymphocytes and perpetuate a cycle of chronic inflammation. Smoking also enhances expression of genes known to confer an increased risk of psoriasis, including HLA-Cw6, HLA-DQA1*0201 and CYP1A1. Improved understanding of the possible link between smoking and psoriasis pathogenesis may provide further insight into mechanisms underlying smoking, psoriasis and risk of subsequent cardiovascular disease.