Gut Microbiota as a Mediator Between Intestinal Fibrosis and Creeping Fat in Crohn's Disease

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Intestinal stricture remains one of the most challenging complications in Crohn's disease, and its underlying mechanisms are poorly understood. Accumulating evidence suggests that gut microbiota is significantly altered in stenotic intestines and may play a key role in the development of fibrogenesis in Crohn's disease. Additionally, the presence of hypertrophic mesenteric adipose tissue, also known as creeping fat, is closely correlated with intestinal stricture and fibrosis. Recent findings have revealed that bacterial translocation to creeping fat might exacerbate colitis and promote intestinal fibrosis. However, there is still a gap in determining whether gut microbiota links the formation of creeping fat to intestinal fibrosis. Hence, this review aims to summarize the known microbial influences on intestinal fibrosis, describes the microbial characteristics of creeping fat in Crohn's disease, and discusses the crosstalk between creeping fat-associated dysbiosis and the development of intestinal fibrosis.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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