Published online Jan 14, 2025. doi: 10.3748/wjg.v31.i2.100024
Revised: November 17, 2024
Accepted: November 22, 2024
Published online: January 14, 2025
Processing time: 134 Days and 17.6 Hours
Inflammatory bowel disease, particularly Crohn's disease (CD), has been linked to modifications in mesenteric adipose tissue (MAT) and the phenomenon known as "creeping fat" (CrF). The presence of CrF is believed to serve as a predictor for early clinical recurrence following surgical intervention in patients with CD. Notably, the incorporation of the mesentery during ileocolic resection for CD has been correlated with a decrease in surgical recurrence, indicating the significant role of MAT in the pathogenesis of CD. While numerous studies have indicated that dysbiosis of the gut microbiota is a critical factor in the development of CD, the functional implications of translocated microbiota within the MAT of CD patients remain ambiguous. This manuscript commentary discusses a recent basic research conducted by Wu et al. In their study, intestinal bacteria from individuals were transplanted into CD model mice, revealing that fecal microbiota trans
Core Tip: Some studies have indicated that dysbiosis of the gut microbiota is a significant characteristic in the development of Crohn's disease (CD). However, the functional role of translocated microbiota in the mesenteric adipose tissue (MAT) of CD patients remains ambiguous. Evidence has shown that the translocation of viable microbiota into human MAT can polarize macrophages, leading to adipogenesis within the MAT and contributing to the formation of creeping fat (CrF) in individuals with CD. Nonetheless, it remains an important inquiry to elucidate the role of MAT-associated microbiota in the pathogenesis of CD. This manuscript aims to discuss the article by Wu et al, which explores the potential therapeutic value of fecal microbiota transplantation in the management of CD. Study by Wu et al suggested that the interactions among gut microbiota, MAT hypertrophy, and intestinal fibrosis may mutually reinforce one another in the pathogenesis of CD. Consequently, targeting MAT and CrF may hold promise as a therapeutic strategy for patients suffering from CD.
