Shared Pathophysiology of Inflammatory Bowel Disease and Psoriasis: Unraveling the Connection

Inflammatory bowel disease (IBD) and psoriasis are both chronic autoimmune diseases with a unique set of characteristics. Interestingly, both conditions share considerable overlap in their pathophysiological mechanisms and immune dysregulation. Epidemiological studies validate the relationship by showing a greater prevalence of co-occurrence of the two disorders. At the genetic level, there is a confirmation of a link between shared susceptibility loci and DNA polymorphism, particularly interleukin-23 receptor (IL23R), interleukin-12 subunit beta (IL12B), tumor necrosis factor (ligand) superfamily member 15 (TNFSF15), and signal transducer and activator of transcription 3 (STAT3). In addition, epigenetic factors have a role in genetic predisposition in the development and progression through processes such as DNA methylation and histone modification adding another layer of genetic susceptibility. The relationship between psoriasis and IBD is emphasized by a comparable immunopathogenesis, which involves delicate relationships between the innate and adaptive immune responses. The primary interest is on the T-helper 17 (Th17) cell pathway and the cytokines interleukin-17 (IL-17), interleukin-23 (IL-23), and tumor necrosis factor-alpha (TNF-α). Consequently, both disorders exhibit chronic inflammation and tissue restructuring, resulting from similar cellular and molecular processes. The presence of overlapping pathophysiology highlights the significance of implementing integrated management strategies and employing multidisciplinary techniques for both diagnosis and therapy. Hence, understanding the mutual processes might facilitate the advancement of precise biologic treatments that aim at these commonly shared inflammatory pathways.