While the exact mechanisms are not yet fully understood, emerging evidence suggests an association between smoking and psoriasis. The components of tobacco can potentially trigger systemic inflammation, thereby exacerbating the inflammatory processes already at work in psoriasis. Observational studies have shown a high prevalence of psoriasis among smokers, reinforcing the hypothesis of a relationship between the two.
The data suggests that smoking can influence the severity of psoriasis. Smokers with psoriasis are likely to develop severe forms of the disease. Interleukins IL-1β, IL-1β ⁄ IL-6, and TGF-β ⁄ IL-21 induce the expression of Th17 lymphocytes. Moreover, it has been demonstrated that tobacco smoke extract was capable of increasing Th17 expression in the presence of these cytokines. Indeed, tobacco smoke could induce the differentiation of Th17 lymphocytes, leading to the expression of IL-17 and IL-22.
Another study has shown that the combination of being a smoker and carrying the HLA-Cw6 gene was about 11 times higher than in non-smokers without the HLA-Cw6 gene. However, the mechanism to justify these observations has not yet been established. Furthermore, it has been shown that nicotine induces an increase in the secretion of several cytokines such as interleukin (IL)-12, tumor necrosis factor (TNF), and IL-2, which are involved in the pathogenesis of psoriasis.
For individuals who smoke and suffer from psoriasis, it is crucial to understand the potential risks. Quitting smoking improves skin health and reduces the severity of symptoms. For this, consulting a healthcare professional is advisable to obtain support and advice.