Ulcerative colitis is a chronic, idiopathic condition defined by uninterrupted mucosal inflammation that originates in the rectum and moves proximally through the colon. Alongside Crohn’s disease, it is classified as one of the two primary types of inflammatory bowel disease (IBD). [1] Clinically, ulcerative colitis is characterized by periodic flare-ups of bloody diarrhea, rectal urgency, tenesmus, and abdominal discomfort, all of which can profoundly diminish a patient’s overall quality of life. [2] Fig. 1. show diagrammatic comparison between normal colon and colon affected by ulcerative Colitis. [3] In recent years, the worldwide frequency and prevalence of ulcerative coltis have risen significantly, with a notable surge in emerging industrial nations. This trend underscores the impact of modern lifestyle and environmental shifts on the disease. [4] While the exact cause is still being determined, ulcerative colitis is recognized as a multifactorial condition. It arises from a dynamic interplay between a patient’s genetic profile, environmental stressors, compromised intestinal barrier function, immune system errors, and shifts in the gut microbiome. [5] The breakdown of the intestinal epithelial barrier, coupled with an imbalance in gut microbiota (dysbiosis), triggers a disproportionate immune reaction within the mucosa. This activation of the immune system leads to an elevated release of pro-inflammatory cytokines—notably TNF-α, IL-6, and IL-1β—which are responsible for driving chronic inflammation and subsequent damage to the tissues. [6] Central to this inflammatory cycle is the activation of specific intracellular signaling cascades. In particular, the NF-κB pathway acts as a primary regulator, controlling the expression of genes associated with inflammation and ensuring the continued destruction of the mucosal lining. [7]
Urvashi Gawande*
Sagar Ande
10.5281/zenodo.19016190