Psoriasis and inflammatory bowel disease: links and risks Original paper

What was studied?

This review article investigates the links between psoriasis and inflammatory bowel disease (IBD), including the genetic, immunological, and environmental factors that contribute to the co-occurrence of these conditions. It highlights shared risk factors, including genetic susceptibility loci, immune dysregulation, and microbiota alterations, that drive the pathogenesis of both diseases. Furthermore, the review provides a comprehensive look at the similarities in the immune mechanisms underlying psoriasis and IBD, especially focusing on the IL-23/Th17 immune pathway, which is central to the inflammatory process in both diseases. The study also explores the pharmacological treatments commonly used to manage psoriasis and IBD, discussing the overlap and specificities of treatment regimens.

Who was studied?

The article synthesizes research from various studies on individuals with psoriasis and IBD. It incorporates findings from both human studies and animal models. Patients with psoriasis and those with Crohn’s disease (CD) and ulcerative colitis (UC), the two primary forms of IBD, are the central focus. The review discusses the genetic overlap between these diseases, emphasizing the role of specific genetic loci (e.g., PSORS1 for psoriasis and IL-23R for IBD) that predispose individuals to both conditions. The article also examines the role of the gut microbiome and immune system, with particular attention to inflammatory mediators, immune cells such as T-cells, macrophages, and dendritic cells, and their involvement in the pathogenesis of both psoriasis and IBD.

Most important findings

One of the most important findings from this review is the genetic overlap between psoriasis and IBD, particularly the shared susceptibility loci, such as the PSORS1 locus for psoriasis and IL-23R for IBD. The presence of these shared genetic markers suggests a common genetic pathway that predisposes individuals to both conditions. The review also highlights the significant role of the immune system, particularly the IL-23/Th17 axis, in driving inflammation in both psoriasis and IBD. This immune pathway leads to the activation of T-cells and the production of proinflammatory cytokines, such as IL-17, which contribute to the inflammatory processes in both diseases.

Additionally, the article points out that microbiota dysbiosis plays a crucial role in the pathogenesis of both psoriasis and IBD. In both conditions, there is a shift in the microbial composition, with a reduction in anti-inflammatory bacteria and an increase in proinflammatory microbes. This imbalance exacerbates the inflammatory response and further contributes to disease progression. In terms of treatment, the review reveals that therapies targeting IL-17, such as secukinumab, have shown efficacy in psoriasis but are less effective in IBD, suggesting disease-specific differences in immune responses despite shared pathways.

Key implications

The implications of these findings are significant for both the management and treatment of psoriasis and IBD. Understanding the shared genetic and immune pathways between the two diseases opens the door for more targeted, personalized therapies that address both skin and gut inflammation simultaneously. The identification of the IL-23/Th17 axis as a central player in disease progression suggests that immunomodulatory treatments targeting this pathway could be beneficial in treating both psoriasis and IBD, though the differential response of these diseases to certain treatments, such as anti-IL-17 therapy, requires consideration of disease-specific factors.