Inflammatory bowel disease treatment: Mechanisms to clinical translation (Review)

Inflammatory bowel disease (IBD) is a group of chronic, relapsing and systemic inflammatory disorders primarily affecting the gastrointestinal tract, including Crohn's disease, ulcerative colitis and rarer distinct subtypes such as indeterminate colitis. IBD has shown a marked shift in global epidemiology, with increasing incidence in newly industrialized regions across Africa, Asia and Latin America. The pathogenesis of IBD reflects a complex interplay between genetic susceptibility, mucosal immune dysregulation, intestinal barrier dysfunction, microbial dysbiosis and environmental exposures. Clinically, conventional therapy, including 5‑aminosalicylic acid, corticosteroids and conventional immunosuppressants, is limited by incomplete efficacy and safety concerns. Alternative therapeutic strategies included biological agents (anti‑tumor necrosis factor α, anti‑integrin, anti‑IL‑12/23 and anti‑tumor necrosis factor‑like ligand 1A), small‑molecule inhibitors (JAK inhibitors, tyrosine kinase 2 inhibitors, sphingosine‑1‑phosphate receptor modulators and NLRP3 inhibitors), microbiome‑based interventions (fecal microbiota transplantation, probiotics and engineered microbes) and regenerative approaches (mesenchymal stem cells and intestinal organoids). The present review aimed to summarize mechanistic insights and clinical evidence for established and emerging therapies and discusses current challenges and future directions for individualized, disease‑modifying treatment of IBD.