Smoking and pathogenesis of psoriasis: a review of oxidative, inflammatory and genetic mechanisms

Br J Dermatol. 2011 Dec;165(6):1162-8. doi: 10.1111/j.1365-2133.2011.10526.x. Epub 2011 Nov 2.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Gene Expression Regulation / genetics
  • Humans
  • Immune Tolerance
  • Immunity, Cellular
  • Mice
  • Microvessels / physiology
  • Neovascularization, Pathologic / etiology
  • Nicotine / pharmacology
  • Nicotinic Agonists / pharmacology
  • Oxidants / metabolism
  • Psoriasis / etiology*
  • Psoriasis / immunology
  • Reactive Nitrogen Species / metabolism
  • Skin / blood supply
  • Smoking / adverse effects*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Antioxidants
  • Nicotinic Agonists
  • Oxidants
  • Reactive Nitrogen Species
  • Vascular Endothelial Growth Factor A
  • Nicotine