Gut microbiota and mesenteric adipose tissue interactions in shaping phenotypes and treatment strategies for Crohn's disease

Abstract

In this letter, we commented on the article by Wu et al. We examined the interactions between mesenteric adipose tissue, creeping fat, and gut microbiota in Crohn's disease (CD), a condition marked by chronic gastrointestinal inflammation with a rising global incidence. The pathogenesis of CD involves complex genetic, environmental, and microbial factors. Dysbiosis, which is an imbalance in gut microbial communities, is frequently observed in CD patients, highlighting the pivotal role of the gut microbiota in disease progression and the inflammatory response. Recent studies have shown that mesenteric adipose tissue and creeping fat actively contribute to inflammation by producing proinflammatory cytokines. The relationship between creeping fat and altered microbiota can shift from a potentially protective role to one that encourages bacterial translocation, further complicating disease management. Recent research has suggested that fecal microbiota transplantation could help restore microbial balance, offering a promising therapeutic strategy to improve clinical disease response.

Keywords: Creeping fat; Crohn’s disease; Dysbiosis; Fecal microbiota transplantation; Intestinal barrier; Intestinal microbiota; Mesenteric adipose tissue.

Figure 1

Interactions between mesenteric adipose tissue and the microbiota in Crohn’s disease. Pathogenic bacteria adhere to the intestinal mucosa, thereby disrupting gut barrier integrity and causing bacterial translocation. Inflammatory signals from the microbiota induce the mesenteric adipose tissue to produce additional proinflammatory cytokines, thus sustaining the inflammatory state that characterizes the intestinal environment in Crohn’s disease.