What is the influence of smoking on psoriasis?

The psoriasis is characterised by the presence of red and scaly patches that form on specific areas of the body. These patches can cause itching and irritation, their intensity varying among individuals. They emerge in response to skin inflammation caused by a malfunction of the immune system. T lymphocytes are responsible for the production of inflammatory molecules such as cytokines (IL-17, IL-22, TNF-α, etc.).

These substances stimulate the proliferation of keratinocytes, cells found in the skin. As a result, the normal rate of cell renewal, which would typically take three weeks, is accelerated to just three days. This process leads to a build-up of immature keratinocytes on the skin's surface, increasing the thickness of the outer layer, thus forming a hyperkeratosis.

Genetic predispositions can also be a factor in the onset of psoriasis. At least 30% of psoriasis cases correspond to family forms. Several genes are involved, particularly genetic variances in immunity genes causing an immune system imbalance. Studies have shown that the positivity of the HLA-Cw6 gene is associated with the early onset of psoriasis and the severe progression of the disease. However, further studies need to be conducted to understand the underlying mechanisms.

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. Furthermore, 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, tumour necrosis factor (TNF) and IL-2, which are involved in the pathogenesis of psoriasis.

For individuals who smoke and suffer from psoriasis, it is essential 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 gain support and advice.

• TORII K. & al. Tobacco smoke is related to Th17 generation with clinical implications for psoriasis patients. Experimental Dermatology (2011).

• NALDI L. Psoriasis and smoking: links and risks. Psoriasis: Targets and Therapy (2016).