IJ

Inflammatory bowel disease (IBD) defines a group of diseases, including Crohn’s disease and ulcerative colitis, characterized by chronic inflammation of the gastrointestinal tract. Evidence suggests that visceral adipose tissue, particularly its mesenteric component, influences the course of IBD through its immunomodulatory properties. Mesenteric adipose tissue (MAT) is composed of multiple cell types, including adipocytes, preadipocytes, and immune cells, that collectively regulate energy balance and endocrine signaling. MAT is a unique fat depot as it directly connects along most of the intestinal serosa and harbors the arteries, veins, and lymph nodes that support intestinal function. MAT’s placement at the intestinal barrier serves to contain microbial translocation and support the repair of intestinal epithelium. However, inflammation initiated by obesity or IBD renders it maladaptive, triggering an influx of immune cells that, in turn, release proinflammatory adipokines, cytokines, and chemokines, resulting in local and systemic metabolic effects. Clinical data strongly link the accumulation of inflammatory MAT in the pathology of Crohn’s disease through the development of “creeping fat", a fibrotic, immune-rich tissue that shields the inflamed bowel but can also exacerbate the condition. The inflammatory mediators produced by MAT and the mechanisms by which they aggravate IBD are not well understood. This review synthesizes recent advances in the understanding of the cellular complexity of MAT, emphasizing the bidirectional immune crosstalk between the intestine and the mesentery, and exploring how metabolic or microbial stress drives maladaptive transformation. Finally, we highlight therapeutic strategies that may preserve the reparative functions of MAT while limiting fibrogenic remodeling.