ReviewEuropean journal of immunology2026
Mesenteric Adipose Tissue as a Modulator of Intestinal Inflammation: Mechanistic Insights and Model Systems in Crohn's Disease.
Review in European journal of immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Inflammatory bowel disease, including Crohn's disease (CD) and ulcerative colitis, is becoming increasingly prevalent. Obesity, specifically visceral adiposity, has been identified as a significant risk factor for disease recurrence and complications. A hallmark of CD is the development of "creeping fat", which is characterized by adipocyte hyperplasia and increased adipokine secretion. Under homeostatic conditions, adipose tissue plays a key role in immune regulation through the secretion of adipokines, such as leptin and adiponectin, which modulate JAK/STAT, AMPK, and NF-kB pathways in immune and epithelial cells. However, in obesity and under metabolic stress, mesenteric adipose tissue undergoes immune remodelling marked by macrophage polarization, Th1/Th17 differentiation, and fibroblast reprogramming driven by TNFα, IL-6, and TGF-β1. These changes promote sustained cytokine production, extracellular matrix deposition, and fibrostenotic remodelling of the intestinal wall. This review highlights current evidence linking mesenteric adipose tissue and creeping fat immunometabolism to intestinal inflammation in CD. We outline key cellular and signalling mechanisms that connect mesenteric adipose to mucosal immune dysregulation and discuss emerging experimental models.
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