Cyclooxygenases in Inflammatory Bowel Disease
Authors:-K. Anil Kumar
Abstract-Inflammatory Bowel Disease (IBD) is a long-term condition that presents as Ulcerative Colitis (UC), or Crohn’s Disease (CD) based on its manifestations. It is characterized by inflammation in the small intestine and colon, impacting millions of individuals globally. The development of IBD is influenced by genetic, environmental, and immunological factors. Various pro-inflammatory agents such as TNF-α, IL-1β, IL-6, IL-12, TGF-β, INF-γ, COX-2, and increased reactive oxygen species contribute to significant intestinal damage. Typical symptoms of IBD include fever, abdominal pain, vomiting, diarrhea, weight loss, blood in the stool, and an elevated risk of colon cancer. Changes in colonic motility linked to IBD can worsen discomfort and diarrhea. Prostaglandins, particularly elevated in IBD patients, may modulate these alterations. The enzyme Cyclooxygenase-2, responsible for producing prostaglandins, is targeted in IBD treatment. The role of PGE2 in the pathogenesis of IBD is intricate; while it can have anti-inflammatory effects by inhibiting pro-inflammatory cytokines, it can also act pro-inflammatory in IBD. Dysregulation of PGE2 production in IBD can lead to excess levels in inflamed gut tissue, perpetuating chronic inflammation by attracting immune cells, increasing blood vessel permeability, and causing tissue damage. The context-dependent role of PGE2 in IBD warrants further research for a comprehensive understanding. Modulating PGE2 levels or its signaling pathways may provide potential therapeutic options for managing IBD. This review specifically examines the involvement of Cyclooxygenases and coxibs in treating IBD.
