Department of Dermatology, University of California Davis, Sacramento, CA 95816, USA.
Br J Dermatol. 2011 Dec;165(6):1162-8. doi: 10.1111/j.1365-2133.2011.10526.x. Epub 2011 Nov 2.
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.
最近的研究表明，吸烟可能通过氧化、炎症和遗传机制引发银屑病的发展。吸烟会引发自由基的形成，刺激银屑病中活性的细胞信号通路，包括丝裂原活化蛋白激酶（MAPK）、核因子-κB（NF-κB）和 Janus 激酶/信号转导和转录激活因子（JAK-STAT）。吸烟通过增加活性氧的形成和减少抗氧化剂的基因表达来损害皮肤。尼古丁还刺激先天免疫细胞，这些细胞是银屑病发病机制的重要组成部分，包括树突状细胞、巨噬细胞和角质形成细胞。这些细胞释放细胞因子，激活 T 淋巴细胞，并使慢性炎症持续存在。吸烟还增强了已知会增加银屑病风险的基因的表达，包括 HLA-Cw6、HLA-DQA1*0201 和 CYP1A1。对吸烟与银屑病发病机制之间可能存在的联系的更好理解，可能会进一步深入了解吸烟、银屑病和随后心血管疾病风险的潜在机制。
