Exciting new research from the Department of Life Sciences at the University of Bath, suggests that a hormone – hepcidin – may be the cause of psoriasis.
Iron is an essential trace element, not only for the circulatory system, but also for maintaining healthy skin, where it participates in many cellular processes, including collagen formation, wound healing, and normal immune function. However, too much iron in the skin can be harmful, enhancing the damaging effects of sunlight and causing abnormal proliferation of skin cells, typical of psoriasis. Whilst it has It has long been recognised that psoriasis sufferers have high concentrations of iron in the skin, the significance of this observation has not been fully understood until now.
It turns out that hepcidin – which is produced in the liver - is responsible for controlling how much iron is absorbed from food and later released into the body. Iron metabolism itself is normally controlled by the liver, but this new study suggests that in patients with psoriasis, it is also generated in the skin. Elevated levels of hepcidin were found in skin biopsies of patients with psoriasis, compared with normal controls. In addition, after being exposed to high levels of hepcidin, mice (which have many genetic and physiological similarities to humans) developed a rodent form of psoriasis in which skin cells retained much more iron than was required. This triggered the over-proliferation of skin cells and increased inflammation in the epidermis – both key features of human psoriasis.
The researchers involved in this study believe a drug targeting hepcidin has the potential to dramatically improve treatment options for all psoriasis patients.
Comment
This is an especially important study, which opens up an entirely new therapeutic opportunity for patients with psoriasis. The pathway to a successful drug development based on these findings is, however, a long one. In particular, much more work is needed to fully elucidate the role of hepcidin in the development of human psoriasis. Nevertheless, this is a firm scientific foundation for next steps.
Reference:
Abboud E, Chrayteh D, Boussetta N, et al. Skin hepcidin initiates psoriasiform skin inflammation via Fe-driven hyperproliferation and neutrophil recruitment. Nature Communications 2024; volume 15, Article number: 6718